Heart failure with Normal and Reduced Ejection Fraction – Assessment and Shared Care Management

@#Non-alcoholic fatty liver disease (NAFLD) has become the commonest chronic liver disease in the world. Overall improvement in public health, active screening of blood products, and universal vaccination of hepatitis B have led to a drop in incidence of hepatitis B and C worldwide. NAFLD is strongly associated with metabolic syndrome. With the rise in overweight status and obesity worldwide, it is not surprising that NAFLD is on the rise. Diagnosis of NAFLD requires confirmation of fatty infiltration in liver, as well as liver damage such as elevated liver enzymes and presence of fibrosis. Currently, the best treatment for NAFLD is weight loss, and the proven method would be dieting with regular exercises. Vitamin E and pioglitazoles are promising medications for treating NAFLD, but each medication has their shortcomings. Until more studies are conducted, lifestyle modification remains the only reliable way to treat NAFLD. Family physicians ought to look out for cardiovascular diseases, as well as being vigilant in cancer screening, as NAFLD is associated with higher risks of ischemic heart disease and cancer.

Heart failure with normal and reduced ejection fraction - assessment and shared care management

@#Heart failure (HF) is a common clinical syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. HF may be caused by disease of the myocardium, pericardium, endocardium, heart valves, vessels, or by metabolic disorders. HF due to left ventricular dysfunction is categorized into HF with reduced ejection fraction (with Left Ventricular Ejection Fraction (LVEF) ≤50 percent, known as HFrEF; also referred to as systolic HF) and HF with preserved ejection fraction (with LVEF >50 percent; known as HFpEF; also referred to as diastolic HF.1 A reduced LVEF in systolic heart failure is a powerful predictor of mortality. As many as 40 -50 percent of patients with heart failure have diastolic heart failure with preserved left ventricular function. Overall, there is no difference in survival between diastolic and systolic heart failure that cannot be attributed to ejection fraction. Patients with diastolic heart failure are more likely to be women, to be older, and to have hypertension, atrial fibrillation, and left ventricular hypertrophy, but no history of coronary artery disease.2,3 The pathogenesis of diastolic dysfunction involves abnormalities of active ventricular relaxation and passive ventricular compliance, which lead to ventricular stiffness and higher diastolic pressures. These pressures are transmitted through atrial and pulmonary venous systems, reducing lung compliance. A combination of decreased lung compliance and cardiac output leads to symptoms.

HOME BLOOD PRESSURE MONITORING, BLOOD PRESSURE VARIABILITY

Hypertension is a common chronic disease affecting nearly one-third of the adult population and an important predictor of cardiovascular morbidity and mortality. Blood pressure is inherently variable and depends on an individual’s physiological state and numerous situational factors. Conventional office recordings to diagnose and monitor a patient’s progress and response to treatment is notoriously restrictive. The harmful effects of hypertension are presumed to be due to a prolonged, elevated average BP. Both ambulatory and home blood pressure monitoring are increasingly adopted in clinical practice to eliminate “white coat” and “masked” hypertension and may also be a better prognostic indicator of cardiovascular events than office values. There remain limitations in access and cost to replacing office BP measurements with out-of-office monitoring modalities. Blood pressure also displays a normal circadian variation with nocturnal dipping and a morning surge. Blunted nocturnal dipping and an exaggerated morning surge are thought to correlate with increased cardiovascular events. The pathogenic mechanisms underlying this phenomenon are not well understood. The threshold above which the morning surge becomes pathological is also unclear. More clinical studies targeting treatment of an exaggerated surge are also necessary before clinicians can attribute more weight towards its prognostic importance.