Cardiac valvular disease

Valvular heart disease Serious regurgitant cardiac valvular disease, primarily affecting the mitral, aortic, or tricuspid valves, has been reported in otherwise healthy people who had taken certain anorectic agents in combination for weight loss. The etiology of these valvulopathies has not been established and their course in individuals after the drugs are stopped is not known. 

More autopsy cases of patients with a history of fen-phen use are warranted to document the frequency of combined cardiac valvular disease and pulmonary hypertension. 

Population-based echocardiographic studies in the United States estimate that about 2.5% of the population have moderate to severe valvular dysfunction (1). Of the cardiac valvular disease categories reported, mitral regurgitation was found to be the most prevalent (1.7%), followed by aortic regurgitation and stenosis (0.5% and 0.4% respectively), while mitral stenosis was the least common (0.1%). The incidence of heart disease increased with age (0.7% between age 18 and 44 and 13.3% in subjects 75 years or older). There was a 1.36-fold increase in overall adjusted mortality in patients with valvular dysfunction compared to those without (1). 

Withdrawn in U.S. due to reports of cardiac valvular disease associated with long-term use. 

Counsel persons at highest risk for developing chronic Q fever, especially persons with preexisting cardiac valvular disease or individuals with vascular grafts. 

Adult polycystic kidney disease (APKD) is one of the most common autosomal dominant diseases, affecting about 1/1,000 whites. The key feature of this disease is the progressive accumulation of renal cysts, which ultimately culminate in kidney failure. APKD is responsible for approximately 10% of end-stage renal disease in North America. Patients may also have hypertension, cerebral aneurysms, liver cysts, and cardiac valvular defects. 

Digoxin exhibits strong systolic action and slows heart rate. It is removed from the organism faster than digitoxin. It is used from chronic cardiac insufficiency in decompensated valvular disease of the heart, myocardium overload in arterial hypertension, tachycardia, ventricular fibrillation, and other analogous situations. Synonyms of this drug are cedoxin, lanacordin, lanoxin, and others. 

Acute or chronic failure of the heart may result from disease of the myocardium itself, mainly ischaemic, or an excessive load imposed on it by arterial hypertension, valvular disease or an arteriovenous shunt. The management of cardiac failure requires both the relief of any treatable underlying or aggravating cause, and therapy directed at the failure itself. 

Prasad A, Mehra M, Park M, Scott R, Uber PA, McFadden PM. Cardiac allograft valvulopathy a case of donor-anorexigen-induced valvular disease. Ann Thorac Surg 1999 68(5) 1840-1. 

Heart failure affects an estimated 4.9 million Americans, and approximately 400,000 new case are diagnosed each year (see Chap. 14). Cardiac transplant candidates typically are patients with end-stage heart failure who have New York Heart Association (NYHA) class III or IV symptoms despite maximal medical management and have an expected 1 -year mortality risk of 25% or greater without a transplant. Idiopathic cardiomyopathy and ischemic heart disease account for heart failure in almost 90% heart transplant recipients. Other less common etiologies include valvular disease (4%), retransplantation for graft atherosclerosis or dysfunction (2%), and congenital heart disease (1.5%). 

Most persons with IE have risk factors, such as preexisting cardiac valvular abnormalities. Many types of structural heart disease result in turbulence of blood flow that increases the risk for IE. 

In a broader unselected population referred for nuclear stress testing, Sharir et al. (6) found that the extent of reversible perfusion defect (as expressed by the summed difference score) was the best predictor of subsequent nonfatal myocardial infarction, and was best fit by an exponential curve. Among these patients, 26% had a history of myocardial infarction, and patients with nonischemic cardiomyopathies, valvular disease, or who underwent revascularization within 60 days were excluded. Importantly, even though ejection fraction most powerfully stratified the risk of cardiac death, in patients with an ejection fraction >30% the amount of perfusion defect provided incremental prognostic information. In patients with an ejection fraction of <30%, the rates of cardiac death were high (>4% per year) regardless of the amount of ischemia. 

Indications Central yang insufficiency phlegm rheum disease. Chronic bronchitis, bronchial asthma, pulmonary emphysema, cardiac or nephrotic edema, valvular disease, Basedow s disease, Meniere s disease, neurosis, neurasthenia, hysteria, motion sickness, rheumatoid arthritis, chronic gastritis, chronic nephritis, renal atrophy, hypertension, sinusitis, rhinitis, anemia, conjunctivitis,chronic optic nerve disorders, optic nerve atrophy, and nebula... 

Pathological cardiac hypertrophy develops in response to stresses, and can be concentric, eccentric, or both. An excess pressure load placed on the heart, for example, resulting from uncorrected hypertension or valvular disease, results in concentric hypertrophy. This hypertrophy is initially believed to be adaptive, normalizing systolic wall stress, though it is not clear that hypertrophy is necessary to maintain systolic function in the face of moderately elevated pressure loads. Eccentric hypertrophy results most often from volume loads such as those in valvular insufficiency. Einally, the hypertrophy that occurs in the remote noninfarcted myocardium, as part of the remodeling process following a myocardial infarction, may be both concentric and eccentric. 

Data on the accumulation of 22 1 fatty acids in humans are also available from the work of Svaar who examined autopsy material from 54 hearts selected from Norwegian men, age 20 to 69, who had died suddenly from accidents (Svaar, 1982). These hearts were selected from a larger group on the basis of being without myocardial infarction, severe coronary stenosis, cardiac hypertrophy or valvular disease by macroscopical examination. No focal myocardial lesions were present. A mild to moderate lipidosis was found in 50% of the hearts but this was not correlated with the concentration of 22 1 which was present at less than 1% of the total lipids (Svaar,... 

It provides detailed information on cardiac structure (atrial and ventricular cavity dimensions, areas, volumes, wall thickness, and mass), cardiac function (systolic and diastolic, right and left ventricular wall motion, fractional shortening and ejection fraction, global and regional, and preload and afterload), valvular disease (structure, function, and degree of regurgitation or stenosis), vascular structures, and hemodynamic data. 

Cardiac abnormalities (e.g., pathological heart block, valvular disease, intraventricular conduction defects other than isolated right bundle branch block, angina pectoris, arrhythmia, coronary artery disease). 

Cardiac disease (valvular disease, effusion, myocardial hypertrophy, => Echocardiography, chest film, cardiac MR associated malformation, etc.)... 

Hildner et al. (57) report that as little as 250 mg intravenous tolbutamide has a positive intropic effect in patients with congenital or rheumatic valvular disease without signs of further cardiac involvement. This results in an increase in oxygen consumption. A connection with the supposed relation between use of tolbutamide and fatal cardiac... 

Cardiac Aortic dissection, coronary artery vasospasm, pericarditis, valvular heart disease... 

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