Journal of Universal Surgery

Editorial

Heart failure is a medical syndrome produced by structural and functional deficiencies in myocardium brings about in damage of ventricular filling or the ejection of blood. Congestive Heart Failure is a condition in which the heart cannot pump all the blood returning to it, leading to a backup of blood in the vessels and an increase of fluid in the body's tissues, including the lungs. The maximum cause for HF is reduced left ventricular myocardial function; though, dysfunction of the pericardium, myocardium, endocardium, heart valves or great vessels alone or in combination is also connected with Heart failure. A number of the major pathogenic mechanisms leading to HF are increased hemodynamic load, ischemia-related dysfunction, ventricular alteration, excessive neuro-humoral stimulation, unusual myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, speeded up apoptosis and genetic mutations.

Approximately 5.1 million people in the United States have clinically perceptible heart failure, and the prevalence continues to increase. Heart failure prevalence has keep on stable over the past decades, with additional 650,000 new cases of heart failure cases detected yearly, specifically for individuals better than 65 years of age. Since prevalence is greater in this age group, heart failure incidence is estimated to get worse in the near future. Epidemiological variances have been distinguished. Black men have the highest prevalence rate (1000 person-years) for heart failure and the utmost five-year mortality rate when compared to whites. White women denote the lowest prevalence. Heart failure in non-Hispanic black males and females has a prevalence of 4.5% and 3.8%, respectively, versus 2.7% and 1.8% in non- Hispanic white males and females, respectively. Although survival has improved, the absolute mortality rates for patients with heart failure remain approximately 50% within five years of diagnosis. The survival rate is inverse proportional to the staging strictness of heart failure.

The adaptive mechanisms that may be adequate to sustain the overall contractile performance of the heart at comparatively normal levels become maladaptive when trying to tolerate sufficient cardiac performance. The primary myocardial reaction to chronically increased wall stress is myocyte hypertrophy, death due to apoptosis, and regeneration. This process ultimately leads to remodeling, regularly the eccentric type, and condensed cardiac output, causing a cascade of the neurohumoral and vascular mechanism. Decreased carotid baroreceptor stimulus and renal perfusion will initiate the sympathetic nervous system and Renin-Angiotensin-Aldosterone system.

Sympathetic nervous system initiation will cause increased heart rate and inotropy, leading to myocardial toxicity. Renin-Angiotensin-Aldosterone system stimulation leads to vasoconstriction, increasing afterload (angiotensin II) and hemodynamic modifications, increasing preload (aldosterone). Both BNP and ANP are peptides out from the atria and ventricles in response to heart chamber pressure/volume expansion. These peptides promote natriuresis and vasodilatation. BNP prevents the reabsorption of sodium in the proximal convoluted tubule. It also overwhelms renin and aldosterone release.

Symptoms of heart failure contain those due to excess fluid increase (dyspnea, edema, orthopnea, abdominal distention from ascites, and pain from hepatic congestion) and those due to a decrease in cardiac output (fatigue, weakness) that is most noticeable with physical exertion. Acute and subacute presentations (days to weeks) are deliberated by shortness of breath at rest and/or with exertion, paroxysmal nocturnal dyspnea, orthopnea, and right upper quadrant distress due to acute hepatic congestion (right heart failure). Palpitations, with or without lightheadedness can take place if patient cultivates atrial or ventricular tachyarrhythmias.