Valvular disease

There can be a number of underlying causes of CHE. The most prevalent is the lack of oxygenated blood reaching the heart muscle itself because of coronary artery disease with myocardial infarction (111). Hypertension and valvular disease can contribute to CHE as well, but to a lesser extent in terms of principal causes for the disease. 

Cardiotoxicity may develop at lower than expected cumulative doses of anthracyclines in patients with risk factors like hypertension, preexisting arrhythmias or valvular disease, advanced age, prior irradiation of the mediastinum. 

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. 

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. 

Since arterial emboli formation involves platelet aggregation and leukocyte and erythrocyte inhltration into the fibrin network, the treatment and prophylaxis of arterial thrombi are more difficult. Arterial embolism is treated more successfully with heparin than with the oral anticoagulants. Anticoagulants are useful for prevention of systemic emboli resulting from valvular disease (rheumatic heart disease) and from valve replacement. 

Contraindications Severe aortic or pulmonic valvular disease hypersensitivity to inamrinone or bisulfites. 

Rheumatic mitral valve disease is associated with thromboembolic complications at reported rates of 1.5 to 4.7% per year the incidence in patients with mitral stenosis is approximately 1.5 to 2 times that in patients with mitral regurgitation. The presence of atrial fibrillation is the single most important risk factor for thromboembolism in valvular disease, increasing the incidence of thromboembolism in both mitral stenosis and regurgitation four- to sevenfold. In current practice, patients with nonrheumatic atrial fibrillation at low risk for thromboembolism based on clinical characteristics frequently are treated with aspirin. Warfarin therapy is considered in higher-risk patients, especially those with previous thromboembolism and in whom anticoagulation is not contraindicated due to preexisting conditions. 

Q13 Arterial emboli, which can block blood vessels and cause ischaemia or infarction in the tissues they affect, tend to originate in the left heart and are associated with valvular disease and dysrhythmias. Mitral stenosis is associated with abnormal atrial rhythm, particularly atrial fibrillation. Fibrillation and other rhythm abnormalities in the atria favour blood coagulation, resulting in production of thromboemboli which can move to distant parts of the circulation, such as the cerebral circulation. Thrombi could also form on surfaces of valves distorted by calcification and other abnormalities. In view of the risks of thromboembolism, it is usual to provide anticoagulant therapy to patients with mitral valve problems and atrial fibrillation. 

Q14 Warfarin is an orally active anticoagulant used in the treatment of valvular disease and atrial fibrillation. It is structurally similar to vitamin K, a compound which is required for the synthesis of prothrombin and several other clotting factors in the liver. Warfarin interferes with the actions of vitamin K and so reduces the risk of blood clotting. When taken by mouth, its effect is not immediate and it takes several days to achieve the maximal clinical effect. 

Patients most often have more than one medical problem at a time. For people suffering from mitral valve disease along with hypertension, ACE inhibitors seem to be a good choice, but they re not for anyone who has valvular disease and normal blood pressure. 

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. 

There is some anecdotal evidence that atrioventricular nodal blockade with verapamil or a beta-blocker can also be effective. However, in two cases the addition of a beta-blocker (either atenolol or metoprolol) to treatment with class I antidysrhythmic drugs (cibenzoline in one case and flecainide in the other) did not prevent the occurrence of atrial flutter with a 1 1 response (47). However, the author suggested that in these cases, although the beta-blockers had not suppressed the dysrhythmia, they had at least improved the patient s tolerance of it. In both cases the uses of class I antidysrhythmic drugs was contraindicated by virtue of structural damage, in the first case due to mitral valvular disease and in the second due to an ischemic cardiomyopathy. 

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. 

The determinants of valvulopathy in patients treated with dexfenfluramine have been investigated age and blood pressure can also affect the prevalence of regurgitation (36,37), as can duration of exposure (36). Others have found no correlation between valvular disease associated with appetite suppressants and either dose or duration of drug exposure (29). 

A 52-year-old woman had a transesophageal echocardiogram 1 year before starting to take fen-phen, and had no significant valvular disease. She presented a year later with a new heart murmur and eventually required isolated aortic valve replacement. Pathological evaluation of the excised aortic valve was consistent with that described with fen-phen use. 

A 44-year-old woman who had previously taken appetite suppressants, developed valvular disease consistent with the effects of fen-phen. She had an identical twin who, despite having been treated with the same medication, remained symptom-free and without abnormal echocardiography. Both the patient and her sister took fen-phen for 2 years. However, the patient took a daily dose of fenfluramine of 60-120 mg (and often as much as 240 mg) and phentermine 90 mg (at times 180 mg), whereas her twin sister adhered to the daily amount prescribed (fenfluramine 60 mg and phentermine 24 mg). 

It has been proposed that valvular disease can be attributable to appetite suppressants only if the following criteria are satisfied ... 

Eight of the 24 patients with valvular disease had newly diagnosed pulmonary hjrpertension, although in most cases it was attributable to valvular abnormalities... 

Mangion JR, Habboub AA, Kamat BR, Tam SK. Transesophageal echocardiography with pathological correlation in severe valvular disease associated with fenfluramine-phentermine. Echocardiography 1999 16(1) 27-30. 

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 valves Valvular disease Endothelial, fibroblast PGA Repair, replacement Durability over mechanical devices [29]... 

The first step in the management of chronic heart failure is to determine the etiology (see Table 14—1) and/or any precipitating factors. Treatment of underlying disorders such as anemia or hyperthyroidism may obviate the need for treatment of heart failure. Patients with valvular diseases may derive significant benefit from valve replacement or repair. Revascularization or anti-ischemic therapy in patients with coronary disease may reduce heart failure symptoms. Drugs that aggravate heart failure (see Table 14—3) should be discontinued, if possible. 

Patients with DHF may present with an acute onset of pulmonary edema. There are a number of potential causes for the acute decompensation of these patients, including volume overload, uncontrolled hypertension, acute myocardial ischemia, progressive valvular disease (aortic stenosis), and new-onset or uncontrolled tachyarrhythmias. Treatment strategies for these patients eventually may include the need for surgery, as in the case of valvular disease. 

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%). 

Respiratory symptoms, cough and hemoptysis may occur due to pulmonary infiltrates of Salmonella typhi and secondary pneumococcal infection. Bacteremia leads to focal disease, which presents with osteomyelitis, endocarditis, particularly in valvular disease, meningitis, soft-tissue abscesses, glomerulonephritis and skin lesions. CNS complications, such as meningitis, mental disturbances, delirium or depressed level of consciousness may occur in severe cases. 

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