Heart Failure with Preserved Ejection Fraction: Management Guidelines (From Heart Failure Association of India, Endorsed by Association of Physicians of India)

Heart failure with preserved ejection fraction (HFpEF) accounts for 15–20% of patients with heart failure (HF) in India. Diagnosis is by clinical features supported by biomarkers and echocardiography. Lifestyle modifications, control of risk factors to optimum levels, and treatment of comorbidities are essential in the management of HFpEF. Spironolactone and sacubitril-valsartan [angiotensin receptor neprilysin inhibitor (ARNI)] are beneficial in subsets of HFpEF, especially with lower range of ejection fraction (EF). Sodium-glucose co-transporter-2 inhibitors (SGLT2i)—empagliflozin and dapagliflozin and probably sotagliflozin are the only currently available drugs which have shown benefits in HFpEF, mostly by reducing hospitalizations. The benefit of SGLT2i is evident in both diabetic and nondiabetic subsets. Heart failure with preserved ejection fraction is defined as patients with HF with documented left ventricular ejection fraction (LVEF) equal to or more than 50%.1 Globally, HFpEF accounts for close to 50% of patients presenting with HF. As per the registry data like Trivandrum Heart Failure Registry2 and ASIAN-HF,3 the proportion of HFpEF in our country is approximately 19–25%, which is much lower as compared to that of western population. There is a possibility that many cases go undiagnosed in developing countries like India. The mean age of presentation of patients from India was around 58–68 years, which is about 10 years younger than the data reported from the west. Heart failure with preserved ejection fraction is characterized by elevated left ventricular filling pressures and/or reduced cardiac output either at rest or on exertion. Cardiac output is maintained at the cost of abnormally elevated filling pressure which is responsible for the symptoms and signs. Neurohumoral activation (sympathetic and renin-angiotensin-aldosterone system activation) is present only in a group of HFpEF patients unlike in patients with heart failure with reduced ejection fraction (HfrEF).

Non-invasive assessment of arterial stiffness by pulse-wave velocity correlates with endothelial dysfunction.

BACKGROUND: Pulse-wave velocity is the speed of the blood pressure wave to travel a given distance between two sites of the arterial system and is determined by the elasticity, wall thickness and blood density. Pulse-wave velocity correlates well with arterial distensibility and stiffness and is a useful non-invasive index to assess arteriosclerosis. Arterial endothelial dysfunction is one of the key early events in atherogenesis, preceding structural atherosclerotic changes. This study sought to establish the correlation of non-invasive estimation of arterial wall stiffness by pulse-wave velocity and its association with endothelial dysfunction in subjects at higher risk for atherosclerosis. METHODS AND RESULTS: A total of 102 subjects (60 males and 42 females, mean age 51 years), including those with hypertension (n = 39), type 2 diabetes mellitus (n = 26), concomitant type 2 diabetes mellitus and hypertension (n = 29) and primary dyslipidemia without diabetes mellitus and hypertension (n = 8). Pulse-wave velocity was measured by the Vascular Profiler 1000 (VP-1000) waveform analysis and vascular evaluation system, an automated, non-invasive, screening device. Endothelial function was assessed by flow-mediated dilation of the brachial artery. The brachial-artery diameter was measured on B-mode ultrasound images, with the use of a 7.0 MHz linear-array transducer. Mean brachial artery pulse-wave velocity on the right extremity was 1699 cm/s and on the left 1694 cm/s. Mean flow-mediated dilation in the study subjects was 3.6 +/- 8.4%. Mean brachial artery pulse-wave velocity in the right and left extremities and the higher value of brachial artery pulse-wave velocity of the two extremities showed a negative and significant correlation with flow-mediated dilation of the brachial artery (correlation coefficient r = -0.32, p = 0.001; r = -0.40 p < 0.0001; r = -0.37, p = 0.001, respectively). Mean heart-brachial pulse-wave velocity also showed a negative and significant correlation with flow-mediated dilation of the brachial artery (r = -0.23, p = 0.022). Mean arterial stiffness was 36.2 +/- 22%. Arterial stiffness in the right extremity and the higher value of the two extremities showed a negative and significant correlation with flow-mediated dilation of the brachial artery (correlation coefficient r = -0.31, p = 0.002; r = -0.32, p = 0.001, respectively). CONCLUSIONS: Increased values of pulse-wave velocity reflecting upon arterial stiffness show an excellent correlation with reduced values of brachial artery flow-mediated dilation. We propose that the non-invasive modalities of estimation of the pulse-wave velocity and endothelial function estimation by flow-mediated dilation of brachial artery be used in clinical practice in assessment of pre-clinical atherosclerosis.

Noninvasive assessment of endothelial dysfunction by brachial artery flow-mediated dilatation in prediction of coronary artery disease in Indian subjects.

BACKGROUND: A noninvasive technique for testing endothelial function by ultrasound measurement of flow-mediated dilatation has recently generated considerable interest as a marker of atherosclerosis, and in the prediction of clinical coronary events and coronary artery disease. METHODS AND RESULTS: We measured the flow-mediated dilatation of the brachial artery (endothelium-dependent vasodilatation) in 136 subjects, with or without evidence of coronary artery disease. Endothelial dysfunction was diagnosed if flow-mediated dilatation was less than 4.5%. Of the 136 subjects (age group 40-70 years) recruited for the study, 94 were males and 42 females. Sixty-eight subjects had evidence of coronary artery disease as diagnosed by documented hospitalization due to myocardial infarction or acute coronary syndrome, proved by coronary angiography when feasible or noninvasive cardiac evaluation. Endothelial dysfunction was detected in 90 subjects (66.2%). Prevalence of coronary artery disease was higher among subjects with endothelial dysfunction compared to those without (57.5% v. 34.7%, p=0.013). Prevalence of endothelial dysfunction was significantly higher among subjects with coronary artery disease as compared to those without coronary artery disease (76.4% v. 55.8%, p=0.012). The present study showed a sensitivity of 76%, specificity of 44%, positive predictive value of 58% and negative predictive value of 65% for endothelial dysfunction in the prediction of coronary artery disease. Multiple regression analysis using coronary artery disease as a dependent variable revealed a statistically significant association with endothelial dysfunction (p=0.033) even after the inclusion of traditional risk factors into the model. CONCLUSIONS: We conclude that endothelial dysfunction shows a strong association with coronary artery disease and can be a useful noninvasive tool for the evaluation of coronary artery disease.