#ventricular ejection

[er-cryptid]

Ventricular Ejection

-- follows isovolumetric ventricular contraction

-- both ventricles continue to contract

-- the ventricular pressures exceed aortic and pulmonary arterial pressure

-- the aortic valve and pulmonary valve open

-- blood is ejected into aorta and pulmonary artery

[wamathai]

AstraZeneca partners with Tricog Health and KCS to promote AI-Powered heart failure screening

AstraZeneca has partnered with Tricog Health, an innovator in AI-driven healthcare solutions, and the Kenya Cardiac Society (KCS) to conduct a groundbreaking study evaluating the effectiveness of an AI-based Left Ventricular Ejection Fraction (LVEF) model in screening for heart failure (HF). Launched in May 2024, the study is being conducted across seven centers in Kenya, strategically selected…

[covid-safer-hotties]

Reference included in our archive

I thought there were some interesting statistics here even thought it's a small study: Almost 1/4 of subjects developed myocarditis *after* recovering from covid.

Abstract Although COVID-19 is a disease consisting of mostly upper and lower respiratory symptoms, a subset of patients develop cardiac sequelae including myocarditis and pericarditis. For these patients, a standardized set of diagnostic imaging techniques and treatments has not been established. While there have been numerous case reports on this topic, there are few reviews that evaluate the effectiveness of different treatment modalities with a significant number of cases. We reviewed 146 cases of patients (ages ranging from 2 months old to mid 80 s) obtained from searches on PubMed, Google Scholar, and several case report journals. ECG abnormalities, elevated inflammatory markers, and reduced left ventricular ejection fraction were most associated with COVID-19 myocarditis. While classic symptoms of COVID-19 include upper respiratory symptoms, a subset of patients diagnosed with COVID-19 displayed no signs of respiratory disease at all. In 22% of cases, cardiac sequelae was not present until after the patient recovered from COVID-19. Steroids were given in 57.5% of cases. Cardiac MRI was used in 40.4% of cases for diagnosis of myocarditis. Of all the patients who were treated with ECMO, 82.1% of these patients were able to fully recover. The use of cardiac MRI and transthoracic echocardiogram for diagnosis of COVID-19 myocarditis should be heavily considered in any patient with COVID-19 infection. ECMO, IVIG, steroids, and anticoagulants should also be heavily considered. A randomized controlled trial should be conducted to better associate treatments with outcomes.

[teachingrounds]

Q. What does an atrial septal defect (ASD) sound like on auscultation?

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A. Unlike ventricular septal defects (VSDs), an inter-atrial defect causes no murmur itself. However, a number of adventitious sounds may be associated with it.

- wide and fixed S2, due to the larger-than-normal volume of blood that is sent through the right-sided circulation, causing a later-than-normal closing of the pulmonary valve (the second sound in S2)

- a crescendo-decrescendo early systolic ejection murmur from the pulmonic valve heard best at the right upper sternal border (RUSB)

- a rumbling mid-diastolic murmur from blood rushing through the tricuspid valve heard best at the left lower sternal border (LLSB)

Pro-Tip: S2 is only wide and fixed when pulmonary resistance is low; if the defect remains open long enough, the extra blood flow will increase pulmonary vascular resistance, decreasing blood flow into the lungs and across the ASD, eventually resulting in Eisenmenger Syndrome.

Example courtesy of Thinklabs

[nursingwriter]

Arrhythmias cause irregular hearts beats in ways that can be life-threatening but there are a number of different types of arrhythmias that require different interventions. To determine the facts, this paper reviews the relevant literature to provide the etiology and pathogenesis, prevalence, clinical signs and symptoms, diagnostic pathways and optimal therapeutic approaches for paroxysmal atrial tachycardia, ventricular fibrillation and Brady arrhythmias, followed by a summary of the research and important findings concerning these three disease states in the conclusion. Paroxysmal Atrial Tachycardia Etiology & Pathogenesis. This type of arrhythmia can occur in individuals who have normal hearts as well as in people who have structurally abnormal hearts including those with congenital heart disease, especially following surgical repair of valvular or congenital heart disease (Budzikowski & Rottman 2015). Common causes of the arrhythmia, risk factors, definition of rhythm via EKG findings. Paroxysmal Atrial Tachycardia (PAT) is caused by irregular firing of the electrical signals in the heart's upper chambers which then affects the electrical signals transmitted from the heart's natural pacemaker, the sinoatrial node (Overview of Paroxysmal Atrial Tachycardia 2016). As a result, the heart rate is accelerated which adversely affects the normal blood-pumping processes of the heart and the normal flow of oxygen and blood (Overview of Paroxysmal Atrial Tachycardia 2016). Prevalence/Incidence. In the United States, there are approximately 89,000 new cases of PAT each year and about 570,000 individuals suffer from the condition (Orejarena & Vidailletpersons 1998). This population is comprised of two subgroups: (a) those with PAT as well as (b) those who also suffer from other cardiovascular disease conditions (Orejarena & Vidailletpersons 1998). Clinical Signs & Symptoms. The majority of PAT sufferers do not experience any discernible clinical signs or symptoms; however, in some cases, PAT sufferers may experience any of the follows: Lightheadedness; Dizziness; Heart palpitations; Angina; and, Breathlessness (Overview of Paroxysmal Atrial Tachycardia 2016). In addition, but more rarely, PAT can also cause unconsciousness and/or cardiac arrest (Overview of Paroxysmal Atrial Tachycardia 2016). Diagnostic Pathways. In most cases, an electrocardiogram (ECG) test is used to diagnose PAT (Overview of Paroxysmal Atrial Tachycardia 2016). Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. Although the majority of individuals who experience a PAT will not require any medicinal or interventional therapy, for those who suffer from frequently recurring or severe episodes may require such treatments (Overview of Paroxysmal Atrial Tachycardia 2016). In some cases, vagal maneuvers are prescribed to slow the heart rate; if these methods are inadequate to resolve the condition, pharmacological interventions may be prescribed, including . flecainide (Tambocor) or propafenone (Rythmol) to slow the heart rate (Overview of Paroxysmal Atrial Tachycardia 2016). In extreme cases, a catheter ablation may be required (Overview of Paroxysmal Atrial Tachycardia 2016). In addition, Burke and Laramie (2000) report that beta blockers can also be used to control the heartbeat rate in a majority of episodic paroxysmal atrial tachycardia events. Ventricular fibrillation Etiology & Pathogenesis. This is the most common arrhythmia type and left untreated can be life-threatening within minutes of onset (Gialama & Prezerakos 2014). Ventricular fibrillation (VF) is caused by the erratic firing of electrical impulses from the heart ventricles, limiting the heart's ability to pump sufficient amounts of blood and oxygen (Gialama & Prezerakos 2014). A number of risk factors exist for this condition, including the following: Previous myocardial infarction (MI); Coronary artery disease (CAD); Left ventricular ejection fraction (LVEF) of less than 40% combined with ventricular tachycardia (VT); Prior episode of sudden cardiac arrest (SCA); Family history of SCA or sudden cardiac death (SCD); Personal or family history of certain abnormal heart rhythms such as long QT syndrome (LQTS); Wolff-Parkinson-White syndrome; extremely low heart rates or heart block; VT or VF after a myocardial infarction (MI); Blood vessel abnormalities; History of syncope (fainting episodes of unknown cause); Heart failure (HF); Dilated cardiomyopathy (DCM); Hypertrophic cardiomyopathy (HCM); Significant changes in blood levels of potassium and magnesium (from using certain drugs); Obesity; Diabetes mellitus; Recreational drug abuse; Genetic factors; and, Molecular and other structural heart defects (Gialama & Prezerakos 2014) Prevalence. Although precise numbers are unavailable because a number of VF episodes are not recorded, current estimates indicate that up to 33% of the approximately 300,000 new cases of SCD each year are caused by VF (Goyal & Rottman 2016). This rate equals an incidence of between 0.08-0.016% per year in the adult population of the United States, but even this seemingly modest incidence means that VF accounts for more deaths each year than from lung cancer, breast cancer, or acquired immunodeficiency syndrome (Goyal & Rottman 2016). By contrast, the pediatric and adolescent age groups are estimated to have an annual incidence of 1.3-8.5 cases of VF per 100,000 persons annually, representing about 5% of all deaths in these age groups (Goyal & Rottman 2016). Clinical Signs & Symptoms. The clinical signs and symptoms of VF include the following: Chest pain; Rapid heartbeat (tachycardia); Dizziness; Nausea; Shortness of breath; and, Loss of consciousness (Symptoms of ventricular fibrillation 2016). Diagnostic Pathways. Ventricular fibrillation can be diagnosed using the following methods: Heart monitoring; Electrocardiogram; Blood tests; Chest x-ray; Echocardiogram; Angiogram; and, Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI) (Tests and diagnosis for ventricular fibrillation 2016). Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. According to Gialama and Prezerakos (2014), beta blockers, angiotensin-converting enzyme (ACE) inhibitors, statins and calcium channel blockers can all be used to manage VF. In addition, potassium channel blockers and amiodarone have been shown to be efficacious in the long-term management of ventricular arrhythmias (Gialama & Prezerakos 2014). In some cases, implantable cardioverter defibrillators (ICDs) may be required to moderate the heart beat (Gialama & Prezerakos 2014). Brady Arrhythmias Etiology & Pathogenesis. This type of arrhythmias occurs when the heart fails to beat at least 60 times per minute (Brady arrhythmias 2016). This can be caused by sick sinus syndrome or heart block (Brady arrhythmias 2016). Interventions, though, are not typically required until the heart beat is reduced to fewer than 40 beats per minute (Brady arrhythmias 2016). There are several different types of brady arrhythmias, including (a) sinus bradycardia and (b) atrioventricular electrical impulse conduction delays (these include first-degree atrial-ventricular block; second-degree atrial-ventricular block (Mobitz I and II); and third-degree, or complete heart block (Waldstein & Elias 2001). Prevalence. Sick sinus syndrome, one of the major causes of brady arrhythmias, occurs in approximately one in 600 cardiac patients over the age of 65 years (Semelka & Gera 2013). Clinical Signs & Symptoms. The clinical signs and symptoms of brady arrhythmias include the results of asymptomatic electrocardiograms, heart failure symptoms, near syncope or syncope, central nervous symptoms, or nonspecific and chronic symptoms such as dizziness or fatigue (Vogler & Breithardt 2012). Diagnostic Pathways. Diagnosis of brady arrhythmias is typically accomplished using symptom-rhythm correlations using noninvasive diagnostic studies such as 12-lead electrocardiogram, Holter electrocardiogram, exercise testing, event recorder, or implantable loop recorders; in rare cases, invasive electrophysiologic testing may be required. (Vogler & Breithardt 2012). Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. The short-term treatment for these conditions includes beta and/or calcium channel blockers; long-term interventions for symptomatic brady arrhythmias include cardiac pacing (Vogler & Breithardt 2012). Conclusion The research showed that arrhythmias are caused by different types of condition but all can result in irregular hearts beats that can be life-threatening unless aggressive interventions are implemented. This was shown to be the case especially with ventricular fibrillations. With any type of arrhythmia, though, careful evaluation and diagnosis is required together with appropriate interventions depending on the unique needs of the patient. Although some types of arrhythmias are more common among older adults (i.e., brady arrhythmias), these conditions can affect people of any age, making vigilance an essential and ongoing need. References Brady arrhythmias. Boston Medical Center. . Available: https://www.boston cardiovascular.org/handler.cfm?event=practice, template&cpid=50108. Budzikowski, AS, Rottman, JN. Atrial Tachycardia. Medscape: News and Perspectives. . Available: http://emedicine.medscape.com/article/151456-overview. Burke, MM, Laramie, JA. Primary Care of the Older Adult: A Multidisciplinary Approach. St. Louis, MO: Mosby, 2009. Gialama, F, Prezerakos, P. The Cost Effectiveness of Implantable Cardioverter Defibrillators: A Systematic Review of Economic Evaluations. Applied Health Economics and Health Policy, February 2104, 12(1), 41-45. Goyal, SK & Rottman JN. Ventricular Fibrillation Epidemiology. Medscape. . Available: http://emedicine.medscape.com/article/158712-overview#a6, Orejarena, LA, Vidallet, H. Paroxysmal Supraventricular Tachycardia in the General Population. Journal of the American College of Cardiology 1998, 34(1), 150-157. Semelka, M, Gera, J. Sick Sinus Syndrome: A Review. American Family Physician, May 15, 2013, 67(10), 691 Tests and diagnosis for ventricular fibrillation. Mayo Clinic. . Available: http://www.mayoclinic.org/diseases-conditions/ventricular-fibrillation/basics/tests-diagnosis/con-20034473. Vogler, J, Breithardt, G. Bradyarrhythmias and Conduction Blocks. Rev Esp Cardiol, 2012, 65(7), 37-41. Waldstein, SR, Elias, ME. Neuropsychology of Cardiovascular Disease. Mahwah, NJ: Lawrence Erlbaum Associates, 2001. Read the full article

[technology112]

How effective is CRT in improving symptoms and quality of life in patients with heart failure, and what are the long-term outcomes?

Cardiac Resynchronization Therapy (CRT) is an advanced treatment for patients suffering from moderate to severe heart failure (HF), particularly those with left ventricular dyssynchrony. It involves implanting a specialized device that helps the heart's chambers beat in a more coordinated manner, improving pumping efficiency and reducing heart failure symptoms.

For those considering CRT treatment in India, understanding cost aspects is crucial. You can find more details about CRT-D cost in India here.

How Does CRT Improve Symptoms in Heart Failure Patients?

Heart failure occurs when the heart struggles to pump blood efficiently, leading to fatigue, breathlessness, and fluid buildup. Many heart failure patients develop ventricular dyssynchrony, meaning the left and right ventricles do not contract in a coordinated manner.

How CRT Works

CRT devices (CRT-P for pacing and CRT-D for defibrillation) send electrical impulses to both ventricles, ensuring synchronized contractions. This: ✔ Improves cardiac output (more blood pumped with each beat). ✔ Reduces mitral regurgitation (improves valve function). ✔ Lowers left ventricular workload, slowing disease progression. ✔ Enhances oxygen supply to the body, reducing symptoms.

Clinical Evidence of Symptom Improvement

Studies show CRT significantly reduces heart failure symptoms in nearly 70% of patients: ✅ Improves exercise capacity (measured by 6-minute walk test). ✅ Reduces breathlessness (dyspnea) and fatigue. ✅ Lowers fluid retention and swelling (edema).

🔹 Example: A heart failure patient with severe fatigue and swelling in the legs may notice improved energy levels and reduced fluid buildup within weeks of CRT implantation.

Quality of Life Benefits of CRT

CRT improves the overall well-being of heart failure patients, allowing them to live more active and fulfilling lives.

Key Quality-of-Life Improvements

✔ Increased Physical Activity – Patients can walk longer distances without breathlessness. ✔ Better Sleep Quality – CRT reduces nighttime symptoms, improving sleep. ✔ Enhanced Mental Well-Being – Less fatigue and breathlessness reduce anxiety and depression. ✔ Greater Independence – Patients regain the ability to perform daily tasks without assistance.

Studies Supporting Quality-of-Life Improvement

🔹 A meta-analysis of clinical trials found that patients who received CRT reported a 40% increase in quality-of-life scores compared to those receiving standard heart failure treatment.

How Effective Is CRT in Reducing Hospitalizations and Mortality?

Heart failure often leads to frequent hospitalizations due to worsening symptoms. CRT has been proven to reduce hospital visits and improve survival rates.

CRT and Hospitalization Rates

🔹 The COMPANION trial found that CRT reduced hospitalizations by 35% compared to medical therapy alone. 🔹 Patients with CRT spend fewer days in the hospital each year, lowering healthcare costs.

CRT and Mortality Rates

🔹 The CARE-HF trial showed that CRT reduces the risk of death by 36% over 5 years. 🔹 Patients with CRT have longer life expectancy compared to those receiving only medication.

🔹 Example: A heart failure patient previously hospitalized multiple times a year for fluid overload may experience fewer hospital visits and a lower risk of sudden cardiac death after CRT implantation.

Long-Term Outcomes of CRT

Many patients with CRT experience long-term improvements, but outcomes vary based on individual health conditions.

Positive Long-Term Outcomes

✅ Sustained Symptom Relief – Most patients continue to feel better for years after CRT implantation. ✅ Stable or Improved Ejection Fraction (EF) – Many patients see an increase in left ventricular ejection fraction (LVEF), meaning the heart pumps more efficiently. ✅ Reduced Risk of Arrhythmias – CRT-D devices prevent sudden cardiac arrest in high-risk patients. ✅ Longer Life Expectancy – CRT has been linked to higher survival rates compared to patients on medical therapy alone.

Challenges and Limitations

🔸 30% of patients are "non-responders" – Their symptoms do not improve significantly. 🔸 Device-Related Risks – Potential for infections or lead malfunctions. 🔸 Battery Life – CRT devices need replacement every 5-7 years.

🔹 Example: A patient who receives CRT at age 60 may live a longer, healthier life compared to one relying only on medication.

Factors Influencing CRT Success

1. Best Candidates for CRT

Patients most likely to benefit from CRT include: ✔ Those with moderate to severe heart failure (NYHA Class II-IV). ✔ Patients with reduced ejection fraction (LVEF ≤ 35%). ✔ Those with left bundle branch block (LBBB) and a QRS duration > 150ms.

2. Factors That Improve CRT Effectiveness

✅ Early Implantation – The sooner CRT is implanted, the better the outcomes. ✅ Good Medication Compliance – CRT works best when combined with heart failure medications. ✅ Regular Follow-Ups – Adjusting CRT settings periodically enhances effectiveness. ✅ Lifestyle Modifications – Diet, exercise, and fluid management play a crucial role in long-term success.

Conclusion

How Effective Is CRT for Heart Failure?

✅ Symptom Relief – Reduces breathlessness, fatigue, and fluid retention. ✅ Quality of Life – Improves daily activities, sleep, and emotional well-being. ✅ Reduced Hospitalizations – Lowers emergency visits and heart failure-related admissions. ✅ Longer Life Expectancy – CRT significantly reduces mortality rates.

[pace-hospitals]

Heart Failure: Symptoms, Causes, Types, Diagnosis, Treatment and Prevention

Heart failure, also called congestive heart failure, is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. The four most common causes that are responsible for about two-thirds of congestive heart failure are ischemic heart disease (IHD), chronic obstructive pulmonary disease (COPD), hypertensive heart disease, and rheumatic heart disease (RHD). Difficulty in breathing, extreme tiredness, swelling in ankles and legs, and lightheadedness are common symptoms of heart failure. The treatment aims to relieve systemic and pulmonary congestion and stabilizing hemodynamic status. A cardiologist can treat heart failure.

Heart failure prevalence

Heart failure prevalence worldwide

In the year 2017, approximately 12 lakhs of hospitalizations were due to congestive heart failure. The current prevalence of congestive heart failure is 643.4 lakhs as per the Global Health Data Exchange registry. According to the Framingham Heart Study, the prevalence of heart failure is 8 per 1000 males aged between 50 to 59 years, with an increase to 66 per 1000 males aged 80 to 89. Heart failure incidence in men doubles with each 10-year age increase after the age of 65, whereas in women, the prevalence for the same age cohort, the incidence triples.

Heart failure prevalence in India

Based on disease specific estimates the prevalence of heart failure in India due to coronary heart disease (CAD), hypertension, obesity, diabetes, and rheumatic heart disease (RHD) ranges from 13 lakhs to 46 lakhs with an annual incidence of 4.916 lakhs to 18 lakhs. Because of the lack of surveillance systems to adequately capture the data the incidence and prevalence estimates of heart failure (HF) are unreliable in India.

[myrawjcsmicasereports]

 Resolution of QRS-fragmentation: A case report and review of literature by Zhong Yi, MD in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: It’s not clear whether the resolution of fQRS can be used to assess the effectiveness of cardiac resynchronization therapy defibrillator (CRT-D) in patients of heart failure with reduced ejection fraction (HFrEF).

Case presentation: Here we report a 78-year-old male patient with HFrEF and refractory ventricular tachycardia (VT), who’s 12-lead electrocardiogram (ECG) showed fQRS in leads V1-V6 with QRS duration of 134 ms on admission. Even though the optimized medication of metoprolol, amiodarone, lidocaine, and berberine was given, the recurrent VT and HFrEF were still refractory. For further management, a CRT-D with multipoint pacing (MPP) function (St. Jude Medical, Sylmar, CA) was considered and implanted. It’s very encouraging that no more VTs and fQRS were recorded 9 hours after a CRT-D with MPP function was implanted, and the left ventricle ejection fraction (LVEF) improved significantly later.

Conclusion: CRT-D with MPP is effective in improving the situation of the patient with ischemic cardiomyopathy and HFrEF, and the fQRS resolution can be considered as a sign of its effectiveness.

Keywords: Fragmented QRS; Heart failure; Cardiac resynchronization therapy; Multipoint pacing

Introduction

Fragmented QRS (fQRS) on the 12-lead electrocardiogram (ECG) is defined as the presence of additional notches buried within the QRS, which is widely accepted as a sign of myocardial infarction scar or fibrosis. [1, 2] The fQRS is derived from the abnormality of ventricular depolarization due to ventricular heterogeneity and derangement of ventricular conduction around the infarction zone or scar. [3-5]  And the fQRS is also a sign of left ventricular desynchronization in patients of heart failure with reduced ejection fraction (HFrEF) and the narrow QRS complex (<150 ms). [6] A meta-analysis showed that fQRS on patient’s baseline ECG increased all-cause mortality and major arrhythmic events in HFrEF patients. [7] However, it’s not clear whether the resolution of fQRS is useful to assess the effectiveness of cardiac resynchronization therapy defibrillator (CRT-D) in patients with ischemic cardiomyopathy, especially those CRT-D with multipoint pacing (MPP) function. Here we present an HFrEF patient who had fQRS on his admission ECG and frequent ventricular tachycardia (VT) on his Ambulatory ECG. But no more VT and fQRS were recorded, 9 hours after the implantation of a CRT-D with MPP function. The patient had provided informed consent for publication of this case.

Case presentation

A 78-year-old man presented with a complaint of chest congestion and short of breath lasted for 2 hours on his admission. He had hypertension for 10 years, but his blood pressure was normal on admission without taking any medicine. He had an old myocardial infarction and a coronary artery stent implanted 18 years before, and 2 more stents implanted 10 years before. The patient took a semi-sitting position, the blood pressure was 105/65 mmHg, and the heart rate was 80 bpm. Both lungs were clear, the apex was left out of the normal limit, and slight edema in lower extremities was found. His laboratory examination, including blood routine, hepatic and renal function, electrolyte, coagulation function, and Cardiac troponin I (CTNI), was normal, but the level of brain natriuretic peptide (BNP) elevated to 3082 pg/ml. The ECG showed sinus rhythm, ventricular bigeminy, fQRS in leads V1-V6, QRS duration of 134 ms, and abnormal Q wave in leads V4-V6 (Fig. 1a). His 24-hours Holter monitoring showed 41,320 polymorphic ventricular premature beats (PVCs), which is 42% of the total 98327 beats, and 254 paroxysmal polymorphic VT (Fig. 2a). His chest x-radiography revealed pulmonary congestion, pear-shaped heart and cardio-thoracic proportion of more than 50% (Fig. 3a). His transthoracic echocardiography showed left atrium and ventricle enlargement with the left ventricular end-diastolic diameter of 62 mm; there was a ventricular aneurysm of 5.2×2.0 cm2; there was minor regurgitation of mitral and aortic valves; the left ventricular ejection fraction (LVEF) was 28%. Moreover, no coronary artery or stent stenosis was shown by coronary angiography. We proposed the patient’s primary diagnosis was ischemic cardiomyopathy and HFrEF. Even though the optimized medication of metoprolol, amiodarone, lidocaine, and berberine was given, the recurrent VT and HFrEF were still refractory. For further management, a CRT-D with MPP function (St. Jude Medical, Sylmar, CA) was considered and implanted. It’s very encouraging that 9 hours after the procedure, no VT was monitored again (Fig. 2b); twenty-four hours later, the fQRS was absent and never been recorded after that, and the QRS duration decreased from 134 ms to 122 ms (Fig. 1b). Also, the level of BNP significantly dropped to 357 pg/ml. Furthermore, nine days after the procedure, the LVEF increased to 45%; 30 days later, no pulmonary congestion was found on his Chest x-radiography and the cardio-thoracic proportion improved significantly (Fig. 3b). While, over one year of follow-up, the patient has remained symptom-free of VT and HF.

The patient’s chest x-radiography revealed pulmonary congestion, pear-shaped heart, and cardio-thoracic proportion more than 50% at baseline; (b) There was no pulmonary congestion, and the cardio-thoracic percentage decreased significantly, 30 days after the CRT-D implantation.

Discussion

Considering this patient’s old MI history, we supposed that the possible reason for short of breath on admission was acute myocardial ischemia or acute heart failure. But there was no coronary artery or stent stenosis on his coronary angiography, and the level of CTNI was normal. Combined with clinical signs, chest x-radiography, echocardiographic signs, and elevated levels of BNP, the reason for short of breath was sure to be acute heart failure.

The fQRS is defined as various ‘RSR’ patterns, with or without a Q wave, located in two contiguous leads of a major coronary artery territory. And, the fQRS manifests as an extra R (R’) wave, ≥2 notches in R wave, or ≥2 notches in the down or up-stroke of S wave.[4] It’s reported that fQRS was associated with myocardial infarction scar or fibrosis, and was considered as a sign of old myocardial infarction. [1, 2] The fQRS was also considered as a marker of left ventricular dyssynchrony in HFrEF patients with narrow QRS complex (<150ms). [6] Furthermore, the fQRS was also associated with higher all-cause mortality, and cardiac event rate defined as MI, need for revascularization, VT and cardiac death. [8, 9] The fQRS found in contiguous 3 leads was a significant predictor of the cardiac death or heart failure hospitalization. [9] fQRS increased MAE in HFrEF patients. [7] In this HFrEF patient, the fQRS, with narrow QRS complex of 134 ms, presented on all the 6 precordial leads (V1-V6) on his admission ECG. As it was discussed on the above, the presence of fQRS, with narrow QRS complex on the ECG, was showed that he had left ventricular dyssynchrony caused by myocardial infarction scar or fibrosis. Therefore, our strategy focused on improving the ischemic cardiomyopathy induced HFrEF, and CRT-D with MPP was the best choice for the management of his refractory VT and HFrEF. Practically, the complete resolution of fQRS accompanied by the improvement of HFrEF in a relatively short hospital stay is strong evidence support for the effectiveness of CRT-D with MPP function.

Implantable CRT with MPP is a new quadripolar technology that involves a left ventricle lead with 4 different pacing electrodes and a dedicated device with multiple pacing options. [9] MPP is superior to the conventional biventricular pacing on the improvement of acute cardiac hemodynamics, left ventricle synchronization, and QRS complex narrowing, and all of this manifested as a higher number of acute responders to CRT. [10-12] Therefore, a CRT-D with MPP was implanted in our patient. Then, he had a significant improvement, such as the termination of VT, the narrowing of QRS, the elevation of LVEF, and the relief of HF symptoms.

In conclusion, CRT-D with MPP is very useful in improving the LVEF of the patient with ischemic cardiomyopathy and HFrEF. And the resolution of fQRS may be a sign of the alleviation of HFrEF by using CRT-D with MPP.

[market-insider]

Southeast Asia Pacemakers Market Insights: Detailed Overview of Market Size, Share, Projected Growth

The Southeast Asia pacemakers market size is expected to reach USD 97.67 million by 2030 and is projected to grow at a CAGR of 5.92% from 2024 to 2030, according to a new report by Grand View Research, Inc. South East Asia is witnessing a significant demographic shift towards an older population. Older individuals are more susceptible to heart-related issues, which increases the need for pacemakers. This aging trend is accelerating the demand for devices that help manage heart rhythm disorders. Moreover, the increasing prevalence of cardiovascular diseases, such as arrhythmias and heart block, is a major driver for the market.

South East Asia Pacemakers Market Report Highlights

The external pacemakers segment held the largest share of more than 50.0% in 2023 due to their widespread use is due to their versatility, ease of application, and the immediate, adjustable support they offer.

The conventional pacemakers segment held the largest share of around 60.0% in 2023. These devices have a long track record of effectiveness in treating bradycardia (slow heart rate) and other arrhythmias.

In 2023, the congestive heart failure (CHF) segment dominated the market, capturing a significant 33.18% share.

Hospitals & cardiac centers held the largest share of 42.27% in 2023. The availability of advanced diagnostic tools, surgical facilities, and post-operative care makes hospitals the preferred setting for pacemaker procedures.

For More Details or Sample Copy please visit link @: South East Asia Pacemakers Market Report

A report from the National Library of Medicine published in April 2024 highlights significant variations in heart failure classifications across Southeast Asia. The INTER-CHF study reveals that 39% of heart failure patients in Malaysia and the Philippines have a reduced left ventricular ejection fraction (LVEF) of less than 40%. Conversely, data from the International REPORT-HF registry shows that in Indonesia, and Thailand, the distribution of heart failure types is 59% HFrEF (heart failure with reduced ejection fraction), 18% HFmrEF (heart failure with mid-range ejection fraction), and 23% HFpEF (heart failure with preserved ejection fraction). Additionally, the NHFR (National Heart Failure Registry of India) reports that HFrEF is the most common classification in South Asia, affecting 65% of patients, followed by HFmrEF at 22% and HFpEF at 13%.

Moreover, government initiatives across Southeast Asia play a crucial role in enhancing access to cardiac pacemakers and improving overall cardiovascular care. The governments are upgrading healthcare infrastructure and modernizing hospitals to include advanced cardiac units, improving access to pacemaker treatments. Initiatives like the Philippines' Universal Health Care (UHC) Law enhance coverage and reduce financial barriers, making advanced cardiac care more accessible to a wider population.

List of major companies in the Southeast Asia Pacemakers Market

Boston Scientific Corporation

Medtronic

BIOTRONIK SE & Co. KG

MicroPort Scientific Corporation

Abbott

Lepu Medical Technology(Beijing)Co.,Ltd.

For Customized reports or Special Pricing please visit @: South East Asia Pacemakers Market Report

We have segmented the Southeast Asia pacemakers market based on product, type, application, end-use and country.

[neotia-getwel]

What is the pathophysiology of congestive heart failure?

Pathophysiology of Congestive Heart Failure (CHF):

Congestive heart failure (CHF) is a condition where the heart is unable to pump blood effectively, leading to inadequate blood flow to the body and fluid buildup in the lungs and other tissues. The pathophysiology involves several interconnected mechanisms:

Reduced Cardiac Output: CHF occurs when the heart's pumping capacity (either due to weakened heart muscle or stiffened heart walls) is insufficient to meet the body’s needs, leading to a reduction in cardiac output.

Increased Preload: When the heart cannot pump effectively, blood backs up in the veins (particularly in the lungs in left-sided heart failure) and increases the volume (preload) that the heart has to pump.

Neurohormonal Activation: The body responds to reduced cardiac output by activating compensatory mechanisms like the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. This increases blood pressure and fluid retention, which further strains the heart and worsens heart failure.

Ventricular Remodeling: Chronic stress on the heart causes changes in the structure and function of the heart muscle, known as remodeling. This may involve dilation of the ventricles, thickening of the heart walls, and fibrosis, making the heart less efficient.

Fluid Retention: The kidneys respond to reduced blood flow by retaining salt and water, which worsens fluid buildup (edema) in tissues, leading to symptoms like swelling in the legs and shortness of breath (due to pulmonary congestion).

Decreased Ejection Fraction: In systolic heart failure, the heart's ability to contract is impaired, leading to a low ejection fraction (EF). In diastolic heart failure, the heart’s ability to relax and fill with blood is impaired, often with a preserved EF but reduced overall filling capacity.

These factors lead to a vicious cycle that worsens heart failure symptoms over time, contributing to fluid buildup in the lungs (pulmonary edema) and peripheral tissues (such as in the legs, abdomen, and liver).

If you're concerned about CHF symptoms or diagnosis, it's important to consult healthcare professionals, such as those at Neotia Getwell Multispecialty Hospital, for a comprehensive evaluation and management plan tailored to your condition.

[rahrahkaz]

Data is Power, Ignorance is Bliss

It was about a year and a half ago that Caleb was about the age that we thought he could tolerate a Cardiac MRI without sedation. He did amazing, partly because of him, but also because of the amazing staff that helped him to not be scared. That was on a Tuesday. On Wednesday we spent all morning at our typical coordinated clinic where he sees all of the specialists. The results of the MRI were not yet available. The appointments were difficult for Caleb as things become tougher for him and we grappled with a fairly invasive foot surgery. But what we didn’t know we found out through My Chart at 5:30 am the next morning while I was laying in bed back in Minnesota.

"There is delayed myocardial enhancement starting at the level of the base and extending into the mid chamber noted in the inferior and infero-lateral segments and extending into the antero-lateral segments. There is greater than 50% myocardial involvement."

I broke. I didn’t have much idea of what it meant, but I knew that any cardiac issues at 9 years old, is just far too young. And while I didn’t know the significance of the results, the “greater than 50%” part hit me hard. I knew it wasn’t good.

While I appreciate the immediate gratification of My Chart test results, I was once again left with these results and google until I could talk to our cardiologist. I read things like:

Death of the heart cells

Myocardial involvement is one of the main factors for mortality

Heart failure

And I googled things like:

Life expectancy for a 9-year-old with greater than 50% myocardial involvement

Quality of life with heart failure

Then I got smart and stopped the downward spiral and reached out to our Cardiologist. It’s been extremely important to me that our clinical care team is more than just a group of physicians that we see a few times a year. That is why we endure long travel days to Ohio from Minnesota, so that we can continue the relationships that we have built for so many years. So I texted our Cardiologist and within minutes had a call back. More than that, she was on a morning beach stroll with her husband while on vacation. I will always make sure we have the right people on our care team, people I know will have my back, and more importantly, Caleb and Dunky’s back.

This conversation was extremely beneficial, not because she said, “it’s okay” or “he’ll be okay” or “it’s no big deal” but because it was a conversation of her first listening to me cry, but then she said things like, “I’m so sorry”, “it’s a terrible disease” and “we will start more heart meds now”.

So here we sit a little over one year later with more data for both kids. Caleb has since had 2 more MRIs, he’s moved from watching Disney movies while getting his MRI to listening to Eminem. They are both now on 3 different heart medications (lisinopril, eplerenone and carvedilol) and we are increasing doses periodically as they grow. Caleb’s results are stable, hoping that the meds are helping to not have additional cardiac issues, at least for now. Stable is winning in Duchenne.

Dunky has had one MRI and his initial results were not good either. In fact, his Left Ventricular Ejection Fraction (LVEF) was worse than Caleb’s initial MRI. It read things like “low-normal” instead of “normal” and “approaching 50% myocardial thickness”. Still scary words and scary stuff, but data is power, and I was ready for this news. Thank you, Caleb, for paving the way so I could take this news better. I still cried, I still yelled, I still grieved this news, but I was able to recover a bit sooner. These results caused the Cardiologist to put Dunky on all the same heart meds as Caleb. He will have another MRI in about 6 months. We pray for stabilization in the LVEF (current state was 53%).

I’m grateful for technology, for EMR systems that talk to each other and for access to information. Duchenne is an interesting disease. I feel like we live in a community focused on data, especially with so many clinical trials in place for Duchenne. However, at the same time I feel like we live in a place of ignorance because there is still so much we don’t know about Duchenne. Like the Cardiologist told me while strolling that white sand beach, “there can be a kid with Duchenne in heart failure that stays at that level for years” but I can’t help but think about the 12-year-old with Duchenne that died of heart failure.

Yes, 12-years-old. Caleb turns 11 in two days. This is the unknown. People love to talk about adults with Duchenne that lived into their 30’s, but it seems that there are still far too many kiddos with Duchenne not making it to their 20’s. There is so much we truly don’t know. I went so far to ask at our last appointments “how much longer do you think we have?” and that question couldn’t be answered. They don’t know.

So what do we do with this data, with this power, with this ignorance and with this bliss? We embrace it. We use what data we have to make guided decisions on medications and how we spend our time. We use the unknown to treat life as if we may not get tomorrow. We stand back up when we feel so kicked down. We ask for help, we spoil them, we live our lives in a way that we won’t have regret.

Thank you to this village that helps us on this journey.

10/26/24

[crimsonpublishersgernotology]

Cardiac Metastasis in an Asymptomatic Geriatric Female

Tumors metastatic to the heart (cardiac metastases) are among the least known and highly debated issues in oncology, and few systematic studies are devoted to this topic [1]. Cardiac metastases are considered to be rare; however, when sought for, the incidence seems to be not as low as expected [2]. This case presents a 68-year-old female patient with worsening cardiac function and stage 4 lung cancers. The transthoracic echocardiogram revealed mildly diminished left ventricular ejection fraction of 40-45%, as well as a low-density mass noted in the left atrium with the left interatrial septum intact. Later, a transesophageal echocardiogram was performed and it revealed a 3 x 1.5cm mass in the left atrium which was thought to originate from or near the right superior pulmonary vein. While therapy was showing favorable results towards the lung mass, a cardiac mass was eventually discovered, and treatment was limited due to its position and size. This case shows that cardiac metastases may not be as rare as the literature suggests and can be asymptomatic despite the massive loss of efficient contractile material. It may be practical to monitor for cardiac metastases in lung cancer patients to prevent further metastasis and help guide therapy.

Read more about this aricle: https://crimsonpublishers.com/ggs/fulltext/GGS.000526.php

Read more articles: https://crimsonpublishers.com/ggs/index.php

[rnomics]

IJMS, Vol. 25, Pages 6661: Hypertension and Heart Failure: From Pathophysiology to Treatment

Hypertension represents one of the primary and most common risk factors leading to the development of heart failure (HF) across the entire spectrum of left ventricular ejection fraction. A large body of evidence has demonstrated that adequate blood pressure (BP) control can reduce cardiovascular events, including the development of HF. Although the pathophysiological and epidemiological role of hypertension in the development of HF is well and largely known, some critical issues still deserve to be clarified, including BP targets, particularly in HF patients. Indeed, the management of hypertension in HF relies on the extrapolation of findings from high-risk hypertensive patients in the general population and not from specifically designed studies in HF populations. In patients with hypertension and HF with reduced ejection fraction (HFrEF), it is recommended to combine drugs with documented outcome benefits and BP-lowering effects. In patients with HF with preserved EF (HFpEF), a therapeutic strategy with all major antihypertensive drug classes is recommended. Besides commonly used antihypertensive drugs, different evidence suggests that other drugs recommended in HF for the beneficial effect on cardiovascular outcomes exert advantageous blood pressure-lowering actions. In this regard, type 2 sodium glucose transporter inhibitors (SGLT2i) have been shown to induce BP-lowering actions that favorably affect cardiac afterload, ventricular arterial coupling, cardiac efficiency, and cardiac reverse remodeling. More recently, it has been demonstrated that finerenone, a non-steroidal mineralocorticoid receptor antagonist, reduces new-onset HF and improves other HF outcomes in patients with chronic kidney disease and type 2 diabetes, irrespective of a history of HF. Other proposed agents, such as endothelin receptor antagonists, have provided contrasting results in the management of hypertension and HF. A novel, promising strategy could be represented by small interfering #RNA, whose actions are under investigation in ongoing clinical trials. https://www.mdpi.com/1422-0067/25/12/6661?utm_source=dlvr.it&utm_medium=tumblr

[nursingwriter]

Arrhythmias cause irregular hearts beats in ways that can be life-threatening but there are a number of different types of arrhythmias that require different interventions. To determine the facts, this paper reviews the relevant literature to provide the etiology and pathogenesis, prevalence, clinical signs and symptoms, diagnostic pathways and optimal therapeutic approaches for paroxysmal atrial tachycardia, ventricular fibrillation and Brady arrhythmias, followed by a summary of the research and important findings concerning these three disease states in the conclusion. Paroxysmal Atrial Tachycardia Etiology & Pathogenesis. This type of arrhythmia can occur in individuals who have normal hearts as well as in people who have structurally abnormal hearts including those with congenital heart disease, especially following surgical repair of valvular or congenital heart disease (Budzikowski & Rottman 2015). Common causes of the arrhythmia, risk factors, definition of rhythm via EKG findings. Paroxysmal Atrial Tachycardia (PAT) is caused by irregular firing of the electrical signals in the heart's upper chambers which then affects the electrical signals transmitted from the heart's natural pacemaker, the sinoatrial node (Overview of Paroxysmal Atrial Tachycardia 2016). As a result, the heart rate is accelerated which adversely affects the normal blood-pumping processes of the heart and the normal flow of oxygen and blood (Overview of Paroxysmal Atrial Tachycardia 2016). Prevalence/Incidence. In the United States, there are approximately 89,000 new cases of PAT each year and about 570,000 individuals suffer from the condition (Orejarena & Vidailletpersons 1998). This population is comprised of two subgroups: (a) those with PAT as well as (b) those who also suffer from other cardiovascular disease conditions (Orejarena & Vidailletpersons 1998). Clinical Signs & Symptoms. The majority of PAT sufferers do not experience any discernible clinical signs or symptoms; however, in some cases, PAT sufferers may experience any of the follows: Lightheadedness; Dizziness; Heart palpitations; Angina; and, Breathlessness (Overview of Paroxysmal Atrial Tachycardia 2016). In addition, but more rarely, PAT can also cause unconsciousness and/or cardiac arrest (Overview of Paroxysmal Atrial Tachycardia 2016). Diagnostic Pathways. In most cases, an electrocardiogram (ECG) test is used to diagnose PAT (Overview of Paroxysmal Atrial Tachycardia 2016). Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. Although the majority of individuals who experience a PAT will not require any medicinal or interventional therapy, for those who suffer from frequently recurring or severe episodes may require such treatments (Overview of Paroxysmal Atrial Tachycardia 2016). In some cases, vagal maneuvers are prescribed to slow the heart rate; if these methods are inadequate to resolve the condition, pharmacological interventions may be prescribed, including . flecainide (Tambocor) or propafenone (Rythmol) to slow the heart rate (Overview of Paroxysmal Atrial Tachycardia 2016). In extreme cases, a catheter ablation may be required (Overview of Paroxysmal Atrial Tachycardia 2016). In addition, Burke and Laramie (2000) report that beta blockers can also be used to control the heartbeat rate in a majority of episodic paroxysmal atrial tachycardia events. Ventricular fibrillation Etiology & Pathogenesis. This is the most common arrhythmia type and left untreated can be life-threatening within minutes of onset (Gialama & Prezerakos 2014). Ventricular fibrillation (VF) is caused by the erratic firing of electrical impulses from the heart ventricles, limiting the heart's ability to pump sufficient amounts of blood and oxygen (Gialama & Prezerakos 2014). A number of risk factors exist for this condition, including the following: Previous myocardial infarction (MI); Coronary artery disease (CAD); Left ventricular ejection fraction (LVEF) of less than 40% combined with ventricular tachycardia (VT); Prior episode of sudden cardiac arrest (SCA); Family history of SCA or sudden cardiac death (SCD); Personal or family history of certain abnormal heart rhythms such as long QT syndrome (LQTS); Wolff-Parkinson-White syndrome; extremely low heart rates or heart block; VT or VF after a myocardial infarction (MI); Blood vessel abnormalities; History of syncope (fainting episodes of unknown cause); Heart failure (HF); Dilated cardiomyopathy (DCM); Hypertrophic cardiomyopathy (HCM); Significant changes in blood levels of potassium and magnesium (from using certain drugs); Obesity; Diabetes mellitus; Recreational drug abuse; Genetic factors; and, Molecular and other structural heart defects (Gialama & Prezerakos 2014) Prevalence. Although precise numbers are unavailable because a number of VF episodes are not recorded, current estimates indicate that up to 33% of the approximately 300,000 new cases of SCD each year are caused by VF (Goyal & Rottman 2016). This rate equals an incidence of between 0.08-0.016% per year in the adult population of the United States, but even this seemingly modest incidence means that VF accounts for more deaths each year than from lung cancer, breast cancer, or acquired immunodeficiency syndrome (Goyal & Rottman 2016). By contrast, the pediatric and adolescent age groups are estimated to have an annual incidence of 1.3-8.5 cases of VF per 100,000 persons annually, representing about 5% of all deaths in these age groups (Goyal & Rottman 2016). Clinical Signs & Symptoms. The clinical signs and symptoms of VF include the following: Chest pain; Rapid heartbeat (tachycardia); Dizziness; Nausea; Shortness of breath; and, Loss of consciousness (Symptoms of ventricular fibrillation 2016). Diagnostic Pathways. Ventricular fibrillation can be diagnosed using the following methods: Heart monitoring; Electrocardiogram; Blood tests; Chest x-ray; Echocardiogram; Angiogram; and, Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI) (Tests and diagnosis for ventricular fibrillation 2016). Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. According to Gialama and Prezerakos (2014), beta blockers, angiotensin-converting enzyme (ACE) inhibitors, statins and calcium channel blockers can all be used to manage VF. In addition, potassium channel blockers and amiodarone have been shown to be efficacious in the long-term management of ventricular arrhythmias (Gialama & Prezerakos 2014). In some cases, implantable cardioverter defibrillators (ICDs) may be required to moderate the heart beat (Gialama & Prezerakos 2014). Brady Arrhythmias Etiology & Pathogenesis. This type of arrhythmias occurs when the heart fails to beat at least 60 times per minute (Brady arrhythmias 2016). This can be caused by sick sinus syndrome or heart block (Brady arrhythmias 2016). Interventions, though, are not typically required until the heart beat is reduced to fewer than 40 beats per minute (Brady arrhythmias 2016). There are several different types of brady arrhythmias, including (a) sinus bradycardia and (b) atrioventricular electrical impulse conduction delays (these include first-degree atrial-ventricular block; second-degree atrial-ventricular block (Mobitz I and II); and third-degree, or complete heart block (Waldstein & Elias 2001). Prevalence. Sick sinus syndrome, one of the major causes of brady arrhythmias, occurs in approximately one in 600 cardiac patients over the age of 65 years (Semelka & Gera 2013). Clinical Signs & Symptoms. The clinical signs and symptoms of brady arrhythmias include the results of asymptomatic electrocardiograms, heart failure symptoms, near syncope or syncope, central nervous symptoms, or nonspecific and chronic symptoms such as dizziness or fatigue (Vogler & Breithardt 2012). Diagnostic Pathways. Diagnosis of brady arrhythmias is typically accomplished using symptom-rhythm correlations using noninvasive diagnostic studies such as 12-lead electrocardiogram, Holter electrocardiogram, exercise testing, event recorder, or implantable loop recorders; in rare cases, invasive electrophysiologic testing may be required. (Vogler & Breithardt 2012). Short-term vs. Long-term Therapeutic approach: medicinal vs. interventional therapy routes. The short-term treatment for these conditions includes beta and/or calcium channel blockers; long-term interventions for symptomatic brady arrhythmias include cardiac pacing (Vogler & Breithardt 2012). Conclusion The research showed that arrhythmias are caused by different types of condition but all can result in irregular hearts beats that can be life-threatening unless aggressive interventions are implemented. This was shown to be the case especially with ventricular fibrillations. With any type of arrhythmia, though, careful evaluation and diagnosis is required together with appropriate interventions depending on the unique needs of the patient. Although some types of arrhythmias are more common among older adults (i.e., brady arrhythmias), these conditions can affect people of any age, making vigilance an essential and ongoing need. References Brady arrhythmias. Boston Medical Center. . Available:.org/handler.cfm?event=practice, Budzikowski, AS, Rottman, JN. Atrial Tachycardia. Medscape: News and Perspectives. . Available: http://emedicine.medscape.com/article/151456-overview. Burke, MM, Laramie, JA. Primary Care of the Older Adult: A Multidisciplinary Approach. St. Louis, MO: Mosby, 2009. Gialama, F, Prezerakos, P. The Cost Effectiveness of Implantable Cardioverter Defibrillators: A Systematic Review of Economic Evaluations. Applied Health Economics and Health Policy, February 2104, 12(1), 41-45. Goyal, SK & Rottman JN. Ventricular Fibrillation Epidemiology. Medscape. . Available: http://emedicine.medscape.com/article/158712-overview#a6, Orejarena, LA, Vidallet, H. Paroxysmal Supraventricular Tachycardia in the General Population. Journal of the American College of Cardiology 1998, 34(1), 150-157. Overview of Paroxysmal Atrial Tachycardia. HealthLine. . Semelka, M, Gera, J. Sick Sinus Syndrome: A Review. American Family Physician, May 15, 2013, 67(10), 691-696. Symptoms of ventricular fibrillation. Mayo Clinic. . Available: http://www.mayo clinic.org/diseases-conditions/ventricular-fibrillation/basics/symptoms/con-20034473. Tests and diagnosis for ventricular fibrillation. Mayo Clinic. . Available: http://www.mayoclinic.org/diseases-conditions/ventricular-fibrillation/basics/tests-diagnosis/con-20034473. Vogler, J, Breithardt, G. Bradyarrhythmias and Conduction Blocks. Rev Esp Cardiol, 2012, 65(7), 37-41. Waldstein, SR, Elias, ME. Neuropsychology of Cardiovascular Disease. Mahwah, NJ: Lawrence Erlbaum Associates, 2001. Read the full article

[technology112]

Who are the ideal candidates for CRT, and what criteria determine eligibility for this treatment?

Cardiac Resynchronization Therapy (CRT) is a treatment for heart failure that uses a specialized pacemaker to improve the coordination of heartbeats. CRT is designed for patients with moderate to severe heart failure who have an abnormal heart rhythm, particularly those with delayed electrical conduction that reduces the efficiency of the heart's pumping action.

What is CRT and How Does It Work?

Cardiac Resynchronization Therapy (CRT) is a specialized pacemaker therapy that corrects abnormal electrical conduction in patients with heart failure.

🔹 How CRT Works:

A CRT device (CRT-P: pacemaker or CRT-D: defibrillator) is implanted under the skin.

Leads (wires) are placed in three heart chambers—the right atrium, right ventricle, and left ventricle.

The device sends electrical impulses to synchronize the contraction of the left and right ventricles.

This improves pumping efficiency and reduces heart failure symptoms.

✅ CRT is primarily used in patients with:

Reduced Ejection Fraction (EF) – The heart's pumping ability is weakened.

Delayed Ventricular Activation – Seen in Left Bundle Branch Block (LBBB).

Who Are the Ideal Candidates for CRT?

The ideal candidates for CRT are patients who meet the following criteria:

🔹 1. Patients with Heart Failure (Moderate to Severe Cases)

CRT is most effective in patients with heart failure classified as NYHA Class II, III, or IV (New York Heart Association classification).

💡 NYHA Classifications: ✅ Class I: No symptoms – Not a candidate for CRT. ✅ Class II: Mild symptoms – CRT may be considered. ✅ Class III: Moderate symptoms – CRT is highly recommended. ✅ Class IV: Severe symptoms – CRT can improve quality of life but may not be sufficient alone.

🔹 2. Patients with Reduced Left Ventricular Ejection Fraction (LVEF ≤ 35%)

Ejection Fraction (EF) measures how well the heart pumps blood.

Normal EF: 55% - 70%.

Heart Failure Patients: EF ≤ 35%.

CRT is recommended for patients with an EF of 35% or lower.

🔹 3. Patients with Abnormal Electrical Conduction (Wide QRS Complex ≥ 120-150 ms)

The QRS complex represents ventricular contraction in an ECG.

A prolonged QRS duration (≥120-150 ms) indicates poor heart synchronization.

Left Bundle Branch Block (LBBB) is the most common conduction abnormality that benefits from CRT.

🔹 4. Patients with Sinus Rhythm (Normal Heartbeat Pattern)

CRT works best for patients with a normal sinus rhythm (NSR) and not irregular arrhythmias like atrial fibrillation (AFib).

Some AFib patients may still benefit from CRT if their condition is well-controlled.

🔹 5. Patients Who Are Already on Optimal Heart Failure Medication

CRT is not the first line of treatment for heart failure.

Candidates must have tried medications (beta-blockers, ACE inhibitors, diuretics) with limited improvement.

Eligibility Criteria for CRT

The major eligibility factors include:

✔️ Ejection Fraction (EF) ≤ 35%. ✔️ NYHA Class II, III, or IV heart failure symptoms. ✔️ QRS Duration ≥ 120-150 ms (preferably LBBB pattern). ✔️ Sinus Rhythm (or controlled AFib). ✔️ Stable on heart failure medication for at least 3 months. ✔️ Expected survival of at least 1 year.

🔴 CRT is NOT recommended for:

Patients with EF > 35% (mild heart failure).

Asymptomatic patients (NYHA Class I).

Narrow QRS duration (<120 ms).

Patients with severe organ failure (liver, kidney, or cancer).

Diagnostic Tests to Determine CRT Eligibility

✅ Echocardiogram (ECHO) – Measures ejection fraction (EF) and ventricular function. ✅ Electrocardiogram (ECG/EKG) – Determines QRS duration and conduction abnormalities (e.g., LBBB). ✅ Holter Monitor Test – Evaluates irregular heart rhythms over 24-48 hours. ✅ Cardiac MRI – Provides detailed structural heart images. ✅ Stress Test – Determines functional heart capacity under exertion.

Benefits of CRT for Eligible Patients

🔹 Improved Heart Function – Better synchronization of ventricular contraction. 🔹 Increased Ejection Fraction – Strengthens the heart’s ability to pump blood. 🔹 Reduced Heart Failure Symptoms – Less fatigue, breathlessness, and swelling. 🔹 Lower Risk of Hospitalization – CRT reduces the need for emergency visits. 🔹 Improved Quality of Life – More physical activity and daily functioning. 🔹 Longer Life Expectancy – CRT has been proven to increase survival rates.

Risks and Considerations of CRT

While CRT is generally safe, some risks include:

🔴 Infection at Implantation Site. 🔴 Lead Displacement (Movement of Pacemaker Wires). 🔴 Pacemaker Malfunction. 🔴 Blood Clots at the Implantation Site. 🔴 Failure to Improve Symptoms in Some Patients.

👉 Careful patient selection is necessary to minimize risks.

Conclusion

Who Should Get CRT?

✔️ Patients with EF ≤ 35%. ✔️ Patients with NYHA Class II, III, or IV heart failure. ✔️ QRS Duration ≥ 120-150 ms (preferably LBBB). ✔️ Patients with stable heart failure on medication.

Who Should NOT Get CRT?

❌ Asymptomatic heart failure patients (NYHA Class I). ❌ Patients with EF > 35%. ❌ Patients with narrow QRS duration (<120 ms). ❌ Patients with terminal illnesses.

CRT can significantly improve heart failure symptoms, increase survival, and enhance quality of life if patients are carefully selected. If you or a loved one is experiencing heart failure symptoms, consult a cardiologist to determine if CRT is the right option.

[helthcareheven]

From Concept to Reality: The Beating Heart Patch Market Journey

The beating heart patch market represents advanced therapeutic solutions aiming to restore cardiac function and geometry after myocardial infarction (MI). Beating heart patches are soft, bioresorbable scaffolds seeded with cells that help in cardiac regeneration. The patches are deployed on the heart during minimally invasive surgeries without requiring cardiac bypass. This innovation holds promise to overcome limitations of conventional treatments for MI, such as ventricular remodeling and reduced ejection fraction over time. The global beating heart patch market is estimated to be valued at US$ 223.6 Mn in 2024 and is expected to exhibit a CAGR of 7.6% over the forecast period 2023 to 2030.

The market growth can be attributed to rising geriatric population, growing prevalence of cardiovascular diseases, and the need for advanced treatment alternatives. According to the World Health Organization, cardiovascular diseases cause over 17 million deaths annually and are a major cause of disability. Beating heart patches present an effective option for patients who are not eligible for coronary bypass surgery or left ventricular assist devices. Key Takeaways Key players operating in the beating heart patch market are BIOCARDIA, INC., Athersys, Inc., CorMatrix Cardiovascular, Inc., BD, LifeNet Health, Inc., and Admedus Ltd. These top players accounted for over 40% market share in 2022. BIOCARDIA, INC. leads with its portfolio of autologous cell-based therapies for cardiac repair. Growing private sector investments to support ongoing clinical trials offer significant growth opportunities in the market. Successful clinical results thus far have attracted venture capitalists and pharmaceutical companies looking to gain early access to innovative therapies. Major players are also exploring geographical expansion opportunities in Asia Pacific and Latin America. The large patient pools in developing economies and need for cost-effective treatments provide scope for international partnerships and product adoption. Market drivers Rising economic burden of cardiovascular diseases: The escalating healthcare costs of treating heart attacks, strokes, and other heart conditions has boosted research into cheaper and more durable cardiac repair solutions like beating heart patches. Their ability to prevent recurring hospitalizations makes them attractive. Increasing adoption of regenerative medicine approaches: Beating heart patches present an advanced application of cell-based regenerative strategies. With developments in tissue engineering and greater understanding of biomaterials, such techniques are increasingly gaining ground over traditional device-based or pharmacological interventions. Market restraints High research and production costs: Developing functioning cardiac patches is a technically challenging endeavor that requires extensive preclinical and clinical testing. This makes the overall commercialization costs for these novel products very high. Uncertain reimbursement scenario: Widespread insurance coverage and availability of public funding will determine the true market potential of beating heart patches. Unclear reimbursement policies act as a restraint for companies and limits patient access.

Segment Analysis The beating heart patch market is segmented into biological beating heart patches and synthetic beating heart patches. The biological beating heart patches segment currently dominates the market due to advantages such as better wound healing, and reduced rejection, when compared to synthetic patches. Biological patches are usually made from materials such as pericardium, small intestine submucosa, or collagen. These closely resemble native tissue and encourage natural tissue regrowth. Global Analysis North America is expected to be the fastest growing region in the beating heart patch market during the forecast period. This is attributed to factors such as rising prevalence of cardiovascular diseases, growing demand for advanced surgical procedures, and presence of major players in the region. Additionally, the region has a highly developed healthcare system and favorable reimbursement policies for advanced treatment options. Also, government support for research activities and clinical trials will contribute to market growth.