Best of heart failure

9 449 © Springer Nature Switzerland AG 2019 P. P. Toth, C. P. Cannon (eds.), Comprehensive Cardiovascular Medicine in the Primary Care Setting , Contemporary Cardiology, https://doi.org/10.1007/978-3-319-97622-8_24 Evidence-Based Management of the Patient with Congestive Heart Failure Nicolas W. Shammas 24.1 Epidemiology of Congestive Heart Failure Congestive heart failure (CHF) is the result of either a weak heart muscle (systolic failure) or a stiff ventricle (diastolic failure). Systolic and diastolic failure may coexist in the same patient [ 1 ]. Irrespective of the etiology, it leads to an inadequate amount of oxygenated blood to meet cellular demand. CHF is a growing problem in the United States and par- ticularly in the elderly [ 2 ]. Over half a million cases are diag- nosed on an annual basis with subsequent high mortality [ 3 ] and a large cost to our economic system [ 4 ]. Although less studied, diastolic failure occurs in approxi- mately 30–35% of all patients and 55% of the elderly with CHF [ 5 , 6 ]. Recently heart failure with normal left ventricu- lar function (HFNEF) is a term that has been more widely used than “diastolic heart failure” and describes a heteroge- neous group of patients with a number of pathological mech- anisms [ 7 ]. It is estimated that 50% of HF patients have HFNEF and display similar physiologic and neurohormonal phenotypes to patients with HF and reduced systolic func- tion. Unless more effective acute and preventative therapies are implemented in treating CHF patients, the social burden in treating these patients will continue to rise [ 8 ]. CHF appears to be on the rise in the United States [ 4 , 9 ] and is partly due to the high prevalence of the metabolic syn- drome, diabetes mellitus, hypertension, and obesity [ 10 ]. Although improvement in survival has been noted in the younger heart failure patient over the past two decades, this benefit has not been seen in the elderly and females [ 11 ]. Survival has improved however in both genders over the past 50 years [ 12 ]. 24.2 Pathophysiology of Congestive Heart Failure There are multiple risk factors that lead to injury to the myo- cardium including coronary artery disease (CAD), hyperten- sion, valvular heart disease, diabetes mellitus, congenital heart defects, anemia, metabolic syndrome, cardiotoxins, and alcoholism [ 13 , 14 ]. Left ventricular remodeling with reduction of left ventricular function (as measured by the ejection fraction) and dilatation of the left ventricle subse- quently occurs. The remodeling process is initially an adap- tation mechanism to reduce wall stress and increase cardiac output by hypertrophy of viable myocytes. Hypertrophy, however, eventually leads to an increase in mass-to-volume ratio and premature myocyte cell death [ 15 ]. As the syn- drome of heart failure occurs, a patient presents with fatigue, increased weight, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and chest pain. A reduced left ventricular function increases the risk of arrhythmias and sudden cardiac death as well as pump failure [ 16 , 17 ]. Cardiac remodeling is mediated partly by activation of the renin–angiotensin–aldosterone (RAAS) system and the sym- pathetic nervous system (SNS) (Fig. 24.1 ). Activation of the RAAS system leads to a rise in angiotensin II (AII); sodium retention and myocardial fibrosis mediated by angiotensin II and aldosterone; peripheral vasoconstriction; and endothelial injury [ 18 ], which lead to programmed cell death (apopto- sis), hypertrophy, and fibrosis. AII also promotes aldosterone secretion. In addition, vasoconstrictors such as endothelin-1 and reactive oxygen species (ROS) are increased, and nitric oxide (NO) synthesis and release are reduced, all contribut- ing to vasoconstriction [ 18 – 20 ]. Furthermore, endothelial dysfunction is further impaired by the increase in inflamma- tory markers and cytokines [ 19 , 21 , 22 ]. Elevated sympathetic tone is part of the syndrome of heart failure with elevation of circulating catecholamines and sup- pression of adrenergic receptors [ 23 ]. Adrenaline has direct toxic effect on the myocardium [ 24 ]. Also, it induces cellular 24 N. W. Shammas Midwest Cardiovascular Research Foundation, Davenport, IA, USA