Latest Research News on heart failure : Jan 2022

Epidemiology of heart failure

Analysis of 34 years of follow-up of Framingham Study data provides clinically relevant insights into the prevalence, incidence, secular trends, prognosis, and modifiable risk factors for the occurrence of heart failure in a general population sample. Heart failure was found to be highly prevalent, affecting about 1% of persons in their 50s and rising progressively with age to afflict 10% of persons in their 80s. The annual incidence also increased with age, from about 0.2% in persons 45 to 54 years, to 4.0% in men 85 to 94 years, with the incidence approximately doubling with each decade of age. Women lagged slightly behind men in incidence at all ages. Male predominance was because of a higher rate of coronary heart disease, which confers a fourfold increased risk of heart failure. Heart failure, once manifest, was highly lethal, with 37% of men and 33% of women dying within 2 years of diagnosis. The 6-year mortality rate was 82% for men and 67% for women, which corresponded to a death rate fourfold to eightfold greater than that of the general population of the same age. Sudden death was a common mode of exitus and accounted for 28% of the cardiovascular deaths in men and 14% in women with heart failure. Hypertension and coronary disease were the predominant causes for heart failure and accounted for more than 80% of all clinical events. Factors reflecting deteriorating cardiac function were associated with a substantial increase in risk of overt heart failure. These include low vital capacity, sinus tachycardia, and ECG evidence of left ventricular hypertrophy. Modifiable predisposing risk factors for heart failure include hypertension, impaired glucose tolerance, an elevated total to high-density lipoprotein cholesterol ratio, obesity, and cigarette smoking. In subjects with coronary disease risk increases progressively from angina to recognized myocardial infarctions to unrecognized infarctions in men. In women angina also carried half the failure risk of a myocardial infarction, and in both sexes unrecognized infarctions were at least as dangerous as symptomatic ones. Using simple office procedures and laboratory tests, it is possible to identify high-risk candidates for heart failure early in its course for preventive management before irreversible myocardial damage has occurred.[1]


Economics of chronic heart failure

Chronic heart failure (CHF) is now recognized as a major and escalating public health problem. The costs of this syndrome, both in economic and personal terms, are considerable. The prevalence of CHF is 1–2% and appears to be increasing, in part because of ageing of the population. Economic analyses of CHF should include both direct and indirect costs of care. Healthcare expenditure on CHF in developed countries consumes 1–2% of the total health care budget. The cost of hospitalization represents the greatest proportion of total expenditure. Optimization of drug therapy represents the most effective way of reducing costs. Recent economic analyses in the Netherlands and Sweden suggest the costs of care are rising.[2]


Xamoterol in severe heart failure

516 patients with New York Heart Association class III and IV heart failure despite treatment with diuretics and angiotensin converting enzyme inhibitors were randomised in a double-blind between-group comparison to xamoterol 200 mg (352) or placebo (164) twice daily for 13 weeks. There was no difference between the treatments in loss of clinical signs. Visual analogue scale and Likert scores indicated that breathlessness was less severe with xamoterol, but there was no difference in exercise duration or total work done. Xamoterol reduced maximum exercise heart rate and systolic blood pressure, did not affect the number of ventricular premature beats after exercise, showed no arrhythmogenic activity, and had variable (agonist and antagonist) effects on 24 h heart rate. On intention-to-treat analysis 32 (9·1%) patients in the xamoterol group and 6 (3·7%) patients in the placebo group died within 100 days of randomisation (p=0·02).[3]


Heart Failure with Preserved Ejection Fraction and Therapeutic Approaches: A Systematic Review and Meta-analysis

Aims: Evidence is still lacking regarding optimal treatment for patients with heart failure with preserved ejection fraction (HfPEF). Our objective is to present an individual evaluation for each of the current available heart failure medications using a meta-analytical model.

Methods and Results: Using meta-analytical techniques we assessed the impact of standard systolic heart failure medications on the combined endpoint of all-cause mortality and/or hospitalization for heart failure as a primary endpoint and on mortality and heart failure hospitalization as separate secondary endpoints for patients with HfPEF. Studies were heterogeneous (Q test, p=0.01) and a random effect model was adopted for analysis. A total of 22 randomized and prospective observational studies of 16,802 patients were included; mean follow up duration was 27 months. Only angiotensin converting enzyme inhibitors (ACEIs) significantly reduced the composite end point of all-cause mortality and /or hospitalization for heart failure (HR 0.74 & 95% CI [0.61-0.89], p=0.01). As for all-cause mortality, only ACEIs (HR 0.57 & 95% CI [0.45-0.71], p=0.005), beta blockers (HR 0.63 & 95% CI [0.41-0.98], p=0.03) and statins (HR 0.41 & 95% CI [0.23-0.72], p=0.001) offered a survival benefit. As for hospitalization for heart failure, only digoxin had a significant effect (HR 0.77 & 95% CI [0.61-0.98], p=0.02).                                                                                                                                                                        

Conclusions: Our analysis suggests that ACEI, beta blockers, statin and digoxin as potential medications that can improve outcomes in patients with HfPEF. However, prospective randomized studies are needed to better assess response to these medications.[4]


Left Ventricular Noncompaction: A Rare Cause of Heart Failure in a HIV Patient

Background: Heart failure in patients with human immunodeficiency virus (HIV) is often from dilated cardiomyopathy as a result of HIV itself, drug myotoxicity, secondary infections, or drug-induced atherosclerosis. Left ventricular noncompaction (LVNC) is a rare cardiac congenital abnormality which occurs due to early arrest of endomyocardial morphogenesis.

Case: A 47- year-old female patient with HIV presented with sudden onset shortness of breath and symptoms of congestive heart failure. Echocardiography showed noncompacted endocardium with reduced left ventricular function. She was subsequently diagnosed with LVNC.

Discussion: Multiple etiologies have been implicated in cardiomyopathy among HIV patients. LVNC is a rare cause of left ventricular failure, particularly in this population. Echocardiography plays a pivotal role in the diagnosis. Conclusion: It is often challenging to identify the underlying cause of cardiomyopathy in a patient with HIV. While LVNC is a rare cause of left ventricular failure, typical findings on echocardiography can obviate the need for a more complex evaluative strategy.[5]


Reference

[1] Kannel, W.B. and Belanger, A.J., 1991. Epidemiology of heart failure. American heart journal, 121(3), pp.951-957.

[2] Berry, C., Murdoch, D.R. and McMurray, J.J., 2001. Economics of chronic heart failure. European journal of heart failure, 3(3), pp.283-291.

[3] Xamoterol in Severe Heart Failure Study Group, 1990. Xamoterol in severe heart failure. The Lancet, 336(8706), pp.1-6.

[4] Makki, N. and Mals, A.B., 2014. Heart failure with preserved ejection fraction and therapeutic approaches: A systematic review and meta-analysis. Cardiology and Angiology: An International Journal, pp.332-346.

[5] Gruenebaum, D.D., Kalavakunta, J.K., Cohn, J.M. and Laird-Fick, H.S., 2015. Left Ventricular Noncompaction: A Rare Cause of Heart Failure in a HIV Patient. Journal of Advances in Medicine and Medical Research, pp.270-274.

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