#HFrEF
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Cardiology review
21 days of DAPT, and then clopidogrel alone is ok if mild stroke. Alteplase if 5.5 hours after symptoms. Thrombectomy within 6 hours; but some pts can benefit from thrombectomy within 24 hours of symptoms onset.
Jardiance prevents hospitalization in pts with HFpEF.
Lower to BP no more than 25% in the first hour for pt's with hypertensive emergency.
From Up To Date:
Acute management – Optimal therapy, including the choice of agent and the blood pressure goal, varies according to the specific hypertensive emergency. It is generally unwise to lower the blood pressure too quickly or too much, as ischemic damage can occur in vascular beds that have reset their autoregulatory threshold to the higher level of blood pressure. For most hypertensive emergencies, mean arterial pressure should be reduced by approximately 10 to 20 percent in the first hour and then gradually during the next 23 hours so that the final pressure is reduced by approximately 25 percent compared with baseline. [So it is 25% in 24 hours].
[According to the rationale for the question, it said to lower the BP 25% in 1 hour, then to 160/100 mmHg.}
The major exceptions to modest and gradual blood pressure lowering over the first 24 hours are:
•Acute phase of an ischemic stroke – The blood pressure is usually not lowered unless it is ≥185/110 mmHg in patients who are candidates for reperfusion therapy (table 2) or ≥220/120 mmHg in patients who are not candidates for reperfusion therapy.
•Acute aortic dissection – The systolic blood pressure is rapidly lowered to a target of 100 to 120 mmHg (to be attained in 20 minutes).
•Spontaneous hemorrhagic stroke – The systolic blood pressure can be rapidly reduced if no contraindications exist.
Stop the ACEI 36 hours before starting Entresto in pts you are switching from ACEI to Entresto for HFrEF.
Non-DHP CCBs (verapamil and diltiazem) are not good for pts with HFrEF. The pt already has a poor EF and these meds slow the HR.
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Understanding “HFREF” ICD-10 Classification
The ICD-10 code for HFREF is I50.2 - Systolic (congestive) heart failure. 🔹 I50.20: Unspecified 🔹 I50.21: Acute 🔹 I50.22: Chronic 🔹 I50.23: Acute on chronic
Always code accurately based on the patient's condition! 🩺
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UK Heart Failure Drugs Market 2024: Segmentation, Leaders, and Future Trends
UK heart failure drugs market through the lens of segmentation (drug class, application, etc.) | Leading companies, latest advancements (gene therapy, combination therapies)
UK Heart Failure Drugs Market: A Segmented View for Healthcare Professionals (2024) The UK heart failure drugs market presents a dynamic landscape for healthcare professionals. With an aging population and rising heart disease prevalence, the demand for effective heart failure medications is expected to soar. This report delves into the market segmentation, highlighting key players, recent…
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#CardiovascularHealth#DigitalTherapeutics#GeneTherapy#HeartFailureDrugs#HeartFailureTreatment#HFpEF#HFrEF#PharmaceuticalInnovation#PrecisionMedicine#UKClinicalTrials#UKHealthcare
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Work-related rant here…
I have noticed that a lot of the colleagues in my area let so many "minor" abnormalities slide despite being signals of a larger problem. I have had patients walk in with really obvious abnormalities ongoing for years without any further investigation done. Example: I had a guy come in with a complaint of weight loss and joint pain. His skin looked weird. Did some basic labs - AST was 40, platelets were ~130. Obviously alarm bells started going off, so I checked his ferritin. It was 3500. Did genetic testing to confirm- hereditary hemochromatosis. It took me quite literally one visit to diagnose this man. Here's the annoying part: afterwards, he got me copies of labs from his previous providers. He had mild LFT elevations and mildly low platelets for years. He has been dealing with this, having damage done to his liver, for years because no one thought an AST 40 + PLT 130 was a combination worth investigating, despite his "unexplained" family history of death by liver cancer.
I would love for this to be a one-off event, but it isn't. I inherit "diet controlled" diabetics with double-digit A1Cs, patients with positive HCV ab testing and no follow up, people with a GFR <60 and no mention of kidney disease in their chart or renal dosing performed, HFrEF patients with no ACE-I/SGLT-2/BB etc, and just… ugh! I am so upset about this HH patient that now I all of my frustrations about shoddy local care are coming out. I just want people to pay attention. I feel like I am always cleaning up messes and I am tired of it.
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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.
#Fragmented QRS#Heart failure#Cardiac resynchronization therapy#Multipoint pacing#Journal of Clinical Case Reports Medical Images and Health Sciences#jcrmhs
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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.
#CardioCare#HeartDevices#PacemakerTech#SoutheastAsiaMed#HealthInnovation#CardiacHealth#MedicalDevicesMarket#HeartSupport#HealthcareTrendsAsia#HeartImplants#CardioTechnology#HealthDevices#HeartHealthAsia#SoutheastAsiaHeartCare#PacemakerSolutions
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Empagliflozin
Empagliflozin is an oral medication used primarily in the treatment of type 2 diabetes. Here's a concise overview of key points about empagliflozin:
1. Drug class: It belongs to a class of drugs called sodium-glucose co-transporter 2 (SGLT2) inhibitors.
2. Mechanism of action: Empagliflozin works by helping the kidneys remove excess sugar from the body through urine.
3. Brand names: The most common brand name is Jardiance, manufactured by Boehringer Ingelheim and Eli Lilly.
4. Uses:
- Primary use: Treatment of type 2 diabetes
- Secondary uses: Reducing the risk of cardiovascular death in adults with type 2 diabetes and established cardiovascular disease
- Treatment of heart failure with reduced ejection fraction (HFrEF)
5. Administration: Taken orally, usually once daily.
6. Common side effects: Urinary tract infections, genital mycotic infections, and increased urination.
7. Benefits: Besides glucose control, it has shown cardiovascular and renal protective effects.
8. Contraindications: Not recommended for patients with type 1 diabetes or diabetic ketoacidosis.
Would you like more detailed information on any specific aspect of empagliflozin, such as its efficacy, dosing, or potential drug interactions?
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Innovative Strategies in Heart Failure Management: Elevating Patient Care and Outcomes
Heart failure is a pervasive and life-altering condition that affects millions of individuals globally. Characterized by the heart's inability to pump blood effectively, heart failure can lead to significant morbidity, frequent hospitalizations, and an overall diminished quality of life. The complexity of managing heart failure necessitates a dynamic and comprehensive approach that integrates the latest advancements in medical treatments, lifestyle interventions, patient education, and multidisciplinary care. This article delves into contemporary strategies for managing heart failure, emphasizing the collective commitment required to enhance patient outcomes and transform lives.
The Complex Nature of Heart Failure
Heart failure occurs when the heart is unable to pump blood efficiently, leading to a buildup of fluid in the lungs and other tissues. This condition can result from a variety of causes, including coronary artery disease, high blood pressure, diabetes, and chronic alcohol use. Heart failure is typically categorized into two types: heart failure with reduced ejection fraction (HFrEF), where the heart muscle is weakened and unable to contract properly, and heart failure with preserved ejection fraction (HFpEF), where the heart muscle is stiff and cannot relax adequately.
The symptoms of heart failure, which can include shortness of breath, fatigue, swelling in the legs, and difficulty performing daily activities, often worsen over time. The progressive nature of the disease can lead to recurrent hospitalizations, decreased independence, and a significant impact on patients' mental and emotional well-being.
Advancements in Pharmacological Treatments
The treatment landscape for heart failure has evolved remarkably over the past few decades, with new pharmacological therapies offering significant improvements in patient outcomes. These medications are designed not only to alleviate symptoms but also to target the underlying mechanisms of the disease, thereby slowing its progression and reducing the risk of hospitalization and death.
Angiotensin Receptor-Neprilysin Inhibitors (ARNIs): ARNIs have emerged as a groundbreaking therapy for patients with HFrEF. By simultaneously blocking the effects of angiotensin II and inhibiting the enzyme neprilysin, these drugs help reduce blood pressure, decrease heart strain, and improve overall heart function.
SGLT2 Inhibitors: Initially developed as a treatment for type 2 diabetes, sodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated profound benefits in heart failure management. These medications not only help manage blood sugar levels but also reduce the risk of heart failure hospitalization and cardiovascular death, making them a valuable addition to the treatment arsenal.
Mineralocorticoid Receptor Antagonists (MRAs): MRAs, such as spironolactone and eplerenone, have been shown to significantly improve outcomes in patients with heart failure by reducing fluid retention, decreasing blood pressure, and minimizing the risk of sudden cardiac death.
Ivabradine: For patients with HFrEF who are in sinus rhythm and have a resting heart rate above 70 beats per minute, ivabradine offers an effective means of reducing heart rate and improving heart function, thereby lowering the likelihood of hospitalization.
Device-Based Interventions
In addition to pharmacological treatments, device-based therapies have become a cornerstone of heart failure management, particularly for patients with advanced disease or those at high risk of arrhythmias.
Implantable Cardioverter-Defibrillators (ICDs): ICDs are small devices implanted in the chest that monitor heart rhythms and deliver electric shocks when life-threatening arrhythmias are detected. For patients with heart failure, ICDs can prevent sudden cardiac death and significantly improve survival rates.
Cardiac Resynchronization Therapy (CRT): CRT devices help coordinate the contractions of the heart's chambers, improving the efficiency of the heart's pumping action. This therapy is particularly beneficial for patients with heart failure and a specific type of abnormal heart rhythm known as left bundle branch block (LBBB).
Left Ventricular Assist Devices (LVADs): For patients with severe heart failure who are not candidates for heart transplantation, LVADs offer a life-sustaining option. These mechanical pumps assist the heart in circulating blood throughout the body, significantly extending life expectancy and improving quality of life.
The Crucial Role of Lifestyle Modifications
While medical treatments are essential, lifestyle modifications are equally important in managing heart failure and improving long-term outcomes. Patients are encouraged to adopt heart-healthy habits that can mitigate symptoms, enhance overall health, and reduce the risk of disease progression.
Dietary Adjustments: A heart-healthy diet is a fundamental aspect of heart failure management. Patients are advised to limit sodium intake to reduce fluid retention and avoid foods high in saturated fats, trans fats, and cholesterol to support cardiovascular health. Incorporating a variety of fruits, vegetables, whole grains, and lean proteins can provide essential nutrients and promote heart function.
Regular Physical Activity: Engaging in regular physical activity, tailored to the individual's capabilities and condition, can improve cardiovascular fitness, increase energy levels, and enhance quality of life. Cardiac rehabilitation programs, which offer structured exercise regimens and education, are particularly beneficial for heart failure patients.
Weight Management: Maintaining a healthy weight is crucial for individuals with heart failure, as obesity can exacerbate symptoms and increase the risk of comorbidities. Weight loss strategies, including dietary changes and increased physical activity, are recommended for overweight patients to improve heart function and reduce the burden on the cardiovascular system.
Smoking Cessation: Smoking is a significant risk factor for heart disease and can worsen heart failure. Quitting smoking is one of the most impactful lifestyle changes a patient can make, leading to improved heart function and a reduced risk of complications. Healthcare providers should offer support through counseling, nicotine replacement therapy, and other cessation programs.
Patient-Centered Care and Education
Empowering patients through education and active involvement in their care is essential for optimizing heart failure management. Patients who understand their condition and treatment options are better equipped to make informed decisions and adhere to prescribed therapies.
Comprehensive Education: Providing patients with clear, concise information about heart failure, its symptoms, and the importance of treatment adherence is critical. Education should also cover self-management techniques, such as monitoring weight and recognizing early signs of decompensation, to enable patients to take proactive steps in managing their condition.
Medication Adherence: Adherence to prescribed medications is a key determinant of successful heart failure management. Healthcare providers should work closely with patients to address potential barriers to adherence, such as complex dosing regimens, side effects, and medication costs. Simplifying treatment plans and using reminder tools can help improve adherence rates.
Support Systems: Building a robust support system is vital for heart failure patients. Family members, caregivers, and healthcare professionals can provide emotional support, practical assistance, and encouragement, helping patients navigate the challenges of living with heart failure. Support groups, both in-person and online, can also offer valuable resources and a sense of community.
The Multidisciplinary Approach to Heart Failure Management
The complexity of heart failure necessitates a multidisciplinary approach to care, with collaboration among various healthcare professionals to address the diverse needs of patients. This approach ensures that patients receive comprehensive care that addresses not only their physical symptoms but also their emotional, social, and psychological well-being.
Integrated Care Teams: A successful heart failure management strategy involves the collaboration of cardiologists, primary care physicians, nurses, dietitians, pharmacists, and social workers. These professionals work together to develop personalized care plans, coordinate treatments, and monitor patient progress, ensuring that all aspects of the patient's health are addressed.
Palliative Care Integration: For patients with advanced heart failure, integrating palliative care into the treatment plan can significantly improve quality of life. Palliative care focuses on symptom management, pain relief, and emotional support, helping patients and their families navigate the challenges of advanced disease.
Telehealth and Remote Monitoring: The use of telehealth and remote monitoring technologies has expanded significantly in recent years, offering new opportunities for managing heart failure. These tools allow healthcare providers to monitor patients' vital signs and symptoms in real-time, enabling early intervention and reducing the need for hospital visits. Telehealth also enhances access to care for patients in remote or underserved areas.
The Future of Heart Failure Management
As we look to the future, ongoing research and technological advancements promise to further revolutionize heart failure management and improve patient outcomes.
Personalized Medicine: Advances in genetic research and biomarker identification are paving the way for personalized medicine in heart failure treatment. By tailoring therapies to an individual's genetic makeup and specific disease characteristics, personalized medicine has the potential to optimize treatment efficacy and minimize side effects.
Regenerative Medicine: Research into stem cell therapy and other regenerative treatments offers hope for the future of heart failure management. These therapies aim to repair damaged heart tissue and restore normal heart function, potentially reversing the effects of heart failure.
Artificial Intelligence (AI) and Big Data: The integration of AI and big data analytics into heart failure management is poised to transform the field. AI algorithms can analyze vast amounts of patient data to identify patterns, predict outcomes, and guide treatment decisions, leading to more precise and effective care.
Heart failure management has made significant strides in recent years, with advances in pharmacological treatments, device-based therapies, lifestyle modifications, and patient-centered care all contributing to improved outcomes. However, the journey is far from over. A continued commitment to innovation, education, and multidisciplinary collaboration is essential to further enhance patient care and quality of life. By embracing new technologies, personalized approaches, and a holistic view of patient well-being, we can continue to make meaningful progress in the fight against heart failure and offer hope to millions of individuals around the world.
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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
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Heart Failure: Causes, Symptoms, Risks & Treatment
In this informative blog, Dr. Kartik Bhosale delves into the critical aspects of heart failure, providing a comprehensive exploration of the condition. From the underlying causes and telltale symptoms to the associated risk factors and the latest advancements in treatment, this blog is your gateway to understanding one of the most prevalent cardiovascular issues
Let’s See
What Is Heart failure?
Heart failure, also known as congestive heart failure, occurs when the heart struggles to pump blood effectively to maintain overall health. It can develop gradually or strike suddenly. This condition may be triggered by various heart issues, including blocked arteries, hypertension, heart valve complications, or problems with the heart muscles. Effective management and treatment play a vital role in enhancing the well-being of individuals dealing with heart failure.
What Are The Symtoms Of Heart Failure?
Heart failure symptoms can differ from person to person, but some common signs to watch for include:
Breathlessness: Feeling short of breath, especially when active or lying down, is a common symptom. Some individuals may experience it even at rest.
Fatigue and Weakness: Unusual tiredness and weakness, which can make daily tasks more challenging.
Swelling: Swelling in the legs, ankles, and feet (called edema) is a typical sign of fluid retention, and it can also affect the abdomen.
Heart Palpitations: Experiencing a rapid or irregular heartbeat, often described as heart palpitations.
Persistent Cough or Wheezing: A lingering cough, sometimes accompanied by pink or white phlegm, can indicate fluid buildup in the lungs.
Reduced Exercise Tolerance: Feeling easily fatigued during physical activities and having limitations in your ability to exercise.
Sudden Weight Gain: A quick increase in weight due to fluid accumulation in the body.
Digestive Symptoms: Some individuals with heart failure might have nausea and a decreased appetite.
Cognitive Changes: In more severe cases, heart failure can lead to mental confusion and difficulties with concentration.
What Are The Types of Heart Failure?
Weak Heart Pumping (Systolic Heart Failure): This type of heart failure occurs when the heart’s main pumping chamber, the left ventricle, has difficulty contracting effectively. This leads to a reduced ability to push out an adequate amount of blood with each beat, resulting in a lower ejection fraction. A lower ejection fraction signifies a weaker pumping capability of the heart.
Stiff Heart (Diastolic Heart Failure): Diastolic heart failure occurs when the left ventricle becomes rigid and has difficulty relaxing during the heart’s filling phase (diastole).
Heart Failure Affecting the Lungs (Right-Sided Heart Failure): Right-sided heart failure arises when the right ventricle encounters challenges in effectively pumping blood to the lungs for oxygenation. This condition can result from left-sided heart failure, lung diseases, or other health issues. Common symptoms include swelling in the legs and feet.
Left-Sided Heart Failure: Left-sided heart failure can be further categorized into two subtypes:
Reduced Pumping Power (Heart Failure with Reduced Ejection Fraction – HFrEF): In this type, the left ventricle’s ejection fraction is diminished, indicating a weakened ability to pump blood effectively.
Stiff yet Normally Pumping : HFpEF occurs when the left ventricle maintains normal pumping ability but has difficulty relaxing during the heart’s resting phase (diastole). This stiffness during relaxation hampers the heart’s ability to fill properly.
What Are The Causes Of Heart Failure:
Coronary Artery Disease: CAD takes the spotlight as a leading cause of heart failure. This condition arises when the arteries that supply blood to the heart muscle become narrowed or blocked due to atherosclerosis, resulting in decreased blood flow to the heart muscle.
High Blood Pressure: high blood pressure places continuous stress on the heart, potentially culminating in heart failure over time. It compels the heart to exert extra effort in pumping blood, which can lead to the weakening of the heart muscle.
Faulty Heart Valves (Heart Valve Disorders): Malfunctioning heart valves, like aortic stenosis or mitral regurgitation, can cause heart failure by compelling the heart to labor more to compensate for the valve problem.
Birth-Related Heart Abnormalities: Certain individuals are born with structural heart irregularities that can eventually lead to heart failure.
Diabetes: Diabetes, when poorly managed, can harm blood vessels and nerves that regulate the heart, elevating the risk of heart failure.
Treatment Of Heart Failure:
Heart failure treatment typically combines medications, lifestyle adjustments, and sometimes medical procedures. The specific plan varies based on the cause and severity of the condition.
Medications:
Diuretics: These medications help reduce fluid retention and swelling by increasing urine output.
ACE Inhibitors: ACE inhibitors relax blood vessels and ease the heart’s workload.
ARBs: ARBs have a similar effect to ACE inhibitors and can be an alternative for those who can’t tolerate ACE inhibitors.
Lifestyle Changes:
Heart-Healthy Diet: Embrace a diet low in salt and rich in fruits, vegetables, and whole grains. Monitoring fluid intake may also be necessary.
Regular Exercise: Engaging in supervised physical activity can enhance heart function and overall fitness.
Quit Smoking: Giving up smoking is paramount for heart health.
Medical Procedures:
Pacemaker or ICD : These devices help regulate heart rhythm and can prevent sudden cardiac events.
Coronary Artery Bypass Surgery: If coronary artery disease is a contributing factor, bypass surgery may be required.
Heart Valve Repair or Replacement: Surgical repair or replacement of heart valves may be recommended if valve problems are present.
Risk Factors:
Coronary Artery Disease : Narrowed coronary arteries from atherosclerosis can lead to heart attacks, damaging the heart muscle and raising heart failure risk.
High Blood Pressure : Prolonged high blood pressure stresses the heart, gradually increasing the risk of heart failure.
Uncontrolled Diabetes: Poorly managed diabetes harms blood vessels and nerves, affecting heart function and amplifying heart failure risk.
Tobacco Smoking: Smoking significantly contributes to heart disease, potentially culminating in heart failure.
Excess Weight (Obesity): Carrying extra body weight strains the heart and heightens the risk of heart failure.
Metabolic Syndrome: This cluster of factors, including high blood pressure, elevated blood sugar, excess abdominal fat, and abnormal cholesterol, escalates the risk of heart disease and heart failure.
Heavy Alcohol Consumption: Excessive alcohol intake can damage the heart muscle, increasing susceptibility to heart failure.
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What is the role of dapagliflozin for treatment of heart failure?
Dapagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has historically been used as an anti-diabetic agent in adults with type 2 diabetes mellitus (T2DM) to improve glycemic control.1,2 After expedited drug review via fast track and priority review designations, the Food and Drug Administration (FDA) approved dapagliflozin on May 5, 2020 to reduce the risk of cardiovascular (CV) death and hospitalization due to heart failure (HF) in adults with New York Heart Association (NYHA) class II, III, or IV symptoms and HF with reduced ejection fraction (HFrEF).3 This FDA approval makes dapagliflozin the first SGLT2 inhibitor to be approved for this indication or for use in patients without T2DM.
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Resumen del tratamiento de la insuficiencia cardíaca
Los 10 mensajes principales para llevar a casa 1.La terapia médica dirigida por guías (GDMT) para la insuficiencia cardíaca (IC) con fracción de eyección reducida (HFrEF) ahora incluye cuatro clases de medicamentos, incluidos los iSGLT2. 2.Los iSGLT2 tienen una clase de recomendación 2a en insuficiencia cardíaca con fracción de eyección ligeramente reducida (HFmrEF). Se hacen recomendaciones…
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Virtual Care Team Optimized Heart Failure Medications During Hospitalization#Virtual #Care #Team #Optimized #Heart #Failure #Medications #Hospitalization
NEW ORLEANS — Heart failure medication regimens improved when a virtual specialist team provided recommendations for optimization each day that patients with heart failure with reduced ejection fraction (HFrEF) were in the hospital for any reason, the IMPLEMENT-HF trial showed. Guideline-directed medical therapy (GDMT) improved significantly compared with usual care, with an adjusted difference…
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for those of you not following my descent into mcr related madness on my sideblog. quick check in. I literally thought about gerard way in order to stop panicking on my exam today. So yeah you could say I'm pretty normal
#i didnt study and it showed!! the test was hard#well it was all chill at first then they started asking questions about hfref vs hfpef symptoms and i was. oof#i thought through it tho and think i did okay? ty mx way for the help#maggie goes to college#maggie.txt
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Quality of Life, Treatment Suboptimal in Women With HFrEF - The Cardiology Advisor
Quality of Life, Treatment Suboptimal in Women With HFrEF – The Cardiology Advisor
January 28, 2019
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Device therapy was underused in both men and women, but more so in women.
Although women with heart failure with reduced ejection fraction present with fewer comorbidities and have a higher survival rate, they experience a poorer quality of life and receive suboptimal treatment when compared with men with the same…
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Conflicted
So I got an admission this morning who was super hypoxic. She is a DNR/DNI and VERY sick at baseline. Literally all the problems (HfrEF, COPD, GI bleed, clotting disorder with active DVTs on heparin, PVD, HTN, HLD, GERD, RA, CAD, Afib, breast cancer).
She came to me on a BiPAP barely saturating 83%. The internist said they were concerned about aspiration and I was like "ok then BiPAP actually isn't a good option because it just shoves everything down." She is in Afib with RVR with HRs 140-160s though maintaining her BPs. She is extremely uncomfortable. I confirm that she doesn't want intubation. Then I switch her to high flow nasal cannula and she does better for maybe 20 minutes but ends up getting REALLY hypoxic. She got as low as 69%. So back on BiPAP she goes and she hangs out in the 75-85% range.
Now, interestingly, she is still alert and oriented even with such low saturations. I explain to her that I'll do all the respiratory/medical/non-invasive stuff I can but that ultimately to correct her hypoxia she would need intubation. She declines. I explain that she could die if her oxygen does not improve with BiPAP. She expressed understanding of this. I explain that I can keep giving her all her meds or she could opt to be comfortable. In the comfort case, I'd give her morphine and get rid of anything that doesn't support comfort. She said she wants to be comfortable and see her family.
So, I make her "comfort care", delete all the meds, then call her family and update them. The patient had this interesting affect/realization of "yes I know I've been slowly dying."
The thing I feel conflicted about is that I don't think I did a good enough job explaining her medical options. I kind of laid it out as either "this" (all the things) or "that" (comfort). Really, there can be an in between. I could still continue her antibiotics and such. I'm worried I jumped the gun and didn't explain things well enough. Also feel like I didn't discuss with her that the BiPAP would probably come off at some point. She expressed a wish to see her family and I explained to her that I wasn't sure if she would survive that long. I kept the BiPAP on to at least give her a chance of that.
I have a personal bias that I freely admit where I believe people with severe comorbidities who acutely decompensate should opt for comfort. I know that about myself, for better or worse. And I also know that sometimes when you give patients too many options it is overwhelming. Sometimes you have to be simplistic. I guess what I don't want to happen is have her family come and be like "well you just MADE her comfort when REALLY all she wanted was to breathe better."
When I left, my patient was sleepy after getting morphine but it did help her breathe better. Her tidal volumes are still trash but at least she was getting better saturations. It's not sustainable but at least she is cozy now.
I guess the other thing that pushed me in this direction was that the patient was DNR/DNI. So, she's not unaware of how sick she is. She clearly values a quality of life that doesn't involved unnecessary stuff. ...I just wish I was more explicit.
I guess I don't want it to seem like I gave up on her or didn't try. And I don't want it to seem like I misrepresented what was going on, though I could have been more clear that her respiratory issues could be due to a reversible cause and that she could do better, potentially, though I doubt that with her severe comorbidities.
I mean...she was SO hypoxic and not making improvement. 100% FiO2 on BiPAP. 84% SpO2. Not sustainable.
So. Here is anxiety Poppen, sitting and worrying about it. I shared my concerns with the day team and they said they would readdress everything. It's not like we can't add her meds back on if she wants more workup. It's just...when I sit and think about it...I could have ultrasounded her heart and lungs. I could have done more investigating instead of being like "shit your saturations have been less that 84% basically since you got here (2 hours) this looks like this is it." I literally told her that I was worried she was actively dying and she was like, "I know, I have been."
*sigh* I don't typically take work home with me in this way. I think since I have started my ICU job in February I've had 2 other occasions where I came home being like "did I make the right decision?"
I feel like in her case, with how sick she is as baseline that comfort is the best option. And she said she wanted that. I guess I just feel like I didn't give her enough information to make the most informed decision. :-/
Update/Edit: bless the day team for contacting me and telling me that family was in agreement and that the patient wouldn't want any more intervention. I think this just serves as a learning point for me to be more clear. I can explain in between options without making it complicated. I'll be more diligent about this, especially in emergent situations, in the future.
#pa-c#physician assistant#physician associate#pre-pa#pre paid#critical care#icu medicine#medicine#caspa#originstory#palliative care#palliative medicine
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