Cardiovascular disease is a leading cause of global mortality, necessitating effective strategies for prevention and treatment. The cardiovascular disease continuum concept highlights the progression from risk factors such as hypertension and diabetes mellitus to advanced stages, including heart failure (HF) and death. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, initially developed to manage diabetes, have emerged as effective therapies across all stages of the cardiovascular disease continuum. Numerous cardiovascular outcome trials demonstrate that SGLT2 inhibitors significantly reduce major adverse cardiovascular events and hospitalizations for HF in patients with and without established atherosclerotic cardiovascular disease. Notably, SGLT2 inhibitors have shown remarkable benefits in reducing HF risk, even in patients without diabetes, including those with HF and preserved ejection fraction. Furthermore, recent studies in post–myocardial infarction patients suggest potential benefits in reducing hospitalizations for HF. Despite their widespread use, the precise mechanisms by which SGLT2 inhibitors confer cardiovascular protection remain unclear, suggesting the need for further investigation. In conclusion, SGLT2 inhibitors have revolutionized cardiovascular disease management, offering significant therapeutic potential across a broad spectrum of patients, and are expected to play an increasingly prominent role in both the prevention and treatment of cardiovascular disease.
Obesity is a risk factor for heart failure and cardiovascular disease. Of particular note, over 80% of patients with heart failure with a preserved ejection fraction (HFpEF) are overweight or obese. In this study, we aimed to review the association between obesity and HFpEF. Obese patients with HFpEF exhibit a distinct phenotype. In addition to impaired left ventricular (LV) diastolic function and high filling pressures, obese patients with HFpEF possess other factors that cause elevated LV filling pressure, such as a greater dependence on plasma volume expansion, aggravated pericardial restraint, and increased ventricular interaction. Obesity can contribute to HFpEF through hemodynamic, neurohormonal, inflammatory, and mechanical mechanisms. An increased amount of body fat can induce plasma volume expansion, resulting in chamber remodeling, pericardial restraint, and ultimately elevations in LV filling pressure. Obesity can mediate the activation of sympathetic nervous system signaling and the renin-angiotensin-aldosterone system. These unique pathophysiological characteristics of individuals with both obesity and HFpEF suggest that obesity with HFpEF can be considered a specific phenotype. Future research is expected to clarify effective treatment modalities for obesity-related HFpEF.
Heart failure (HF) in patients with diabetes mellitus has long been considered a consequence of coronary artery disease (CAD). However, recent epidemiological evidence on patients with diabetes showed a significantly increased prevalence of HF in patients with no significant stenosis in the coronary artery. As such, these are thought to be separate entities of diabetic complications. Therefore, HF in patients with diabetes is now considered an independent disease entity of the ‘diabetic heart.’ The mechanism of ‘diabetic heart’ could be due to CAD and diabetic cardiomyopathy caused by altered energy metabolism in the myocardium and advanced glycation end-product accumulation, altered calcium handling, and oxidative stress in the myocardium. Recent cardiovascular outcome trials of anti-diabetic medications have shown the protective effects of certain drugs against HF in patients with and without diabetes. In this review, the relationship between diabetes and the treatment and prevention of HF is summarized.
Hyponatremia is common in hospital setting in patients with heart failure and is associated with increased morbidity and mortality. However, despite these complications, appropriate treatment strategies other than established therapies such as hypertonic saline, loop diuretics, and fluid restriction are limited. Tolvaptan, a vasopressin receptor antagonist, has aquaretic effects that excrete free water and dilutes urine, thereby increasing serum sodium concentration. This new approach might be a landmark in the treatment of hyponatremia as there is a lack of controlled studies in this field. However, regardless of the associated advantage, tolvaptan is recommended to be used for less than 30 days owing to the possibility of liver injury. This study is aimed to present the clinical use of tolvaptan for hyponatremia in patients with heart failure.
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The role of tolvaptan add-on therapy in patients with acute heart failure: a systematic review and network meta-analysis Vireza Pratama, Jordan Budiono, Jarir At Thobari, Bambang Widyantoro, Vita Yanti Anggraeni, Lucia Kris Dinarti Frontiers in Cardiovascular Medicine.2024;[Epub] CrossRef
Heart failure (HF) is an important cardiovascular disease because of the increasing prevalence, high morbidity and mortality, and rapid expansion of health care costs. Over the past decades, efforts have been made to modify the prognosis of patients with HF. Regarding HF with reduced ejection fraction (HFrEF), several drugs have shown to improve mortality and morbidity, based on large-scale randomized controlled trials, leading to a critical paradigm shift in its pharmacological treatment. The paradigm of HFrEF pathophysiology has shifted from cardiorenal disease to hemodynamic changes, and neurohormonal activation is currently considered the prime pathophysiological mechanism of HFrEF. This review summarizes evidence on the pharmacological management of HFrEF derived from major randomized controlled trials, which have accomplished improvements in survival benefits.
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Background The CHA2DS2-VASc score is a popular tool for risk prediction of thromboembolism in patients with atrial fibrillation (AF). Each component of the CHA2DS2-VASc scheme is an established risk factor for left ventricular diastolic dysfunction and heart failure (HF). In AF patients, HF is often adversely affecting to clinical outcomes including thromboembolism. We hypothesized that the CHA2DS2-VASc score reflects cardiac reserve and the risk of HF as well as the risk of stroke in patients with AF.
Methods A total of 103 patients who had the diagnosis of chronic non-valvular AF patients with preserved ejection fraction (EF) were enrolled consecutively. CHA2DS2-VASc score was compared to exercise capacity (peak oxygen uptake, peak VO2), B-type natriuretic peptide (BNP) and echocardiographic diastolic dysfunction index (early mitral to annular velocity, E/E′) ratio.
Results Exercise capacity was correlated with age (β=−0.568, p<0.001), CHA2DS2-VASc score (β=−0.526, p<0.001), BNP (β=−0.449, p<0.001) and diastolic dysfunction (β=−0.534, p<0.001). Patients with CHA2DS2-VASc score ≥2 had a significantly less exercise capacity than those with CHA2DS2-VASc score <2 (p<0.001). Higher CHA2DS2-VASc score was associated with lower exercise capacity, more diastolic dysfunction and higher BNP (for trend p=0.001).
Conclusions High CHA2DS2-VASc score is associated with poor exercise capacity in patients with AF. Diastolic dysfunction is thought to be the major mechanism of exercise limitation. CHA2DS2-VASc score might be useful for predicting overall cardiac reserve as well as stroke risk stratification in AF patients.