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Small deposits of amyloid are often found in the hearts of elderly patients. However, extensive deposition of transthyretin-derived amyloid fibrils in the heart (senile systemic amyloidosis [SSA]) can cause heart failure. The clinical features of SSA that involve the heart are ill defined, and the condition may be overlooked as a cause of heart failure. We sought to better define the clinical, echocardiographic, and electrocardiographic features of cardiac involvement in SSA and to compare them with the findings in patients with light chain-associated (AL) amyloidosis that affects the heart.Eighteen consecutive patients with SSA and heart failure evaluated at a tertiary referral center for the diagnosis and treatment of amyloidosis were compared with 18 randomly selected patients with AL amyloidosis that involved the heart. All patients underwent a complete clinical and biochemical evaluation. Echocardiograms and electrocardiograms were interpreted by blinded investigators.Patients with SSA were older than those with AL amyloidosis and were all male. Proteinuria (protein output of1 g per 24 hours) was common in AL amyloidosis but was not present in SSA. Left ventricular wall thickness was greater in patients with SSA than those with AL amyloidosis, but despite thicker walls and older age, the severity of heart failure was less in the SSA group and the median survival was much longer (75 vs 11 months; P = .003).Senile systemic amyloidosis is a disorder of elderly men and is characterized by amyloidosis clinically limited to the heart. In contrast to the rapid progression of heart failure in AL amyloidosis, SSA results in slowly progressive heart failure. The difference in survival, despite evidence of more myocardial disease in the senile group, suggests that heart failure in AL amyloidosis may have a toxic component, possibly related to the circulating monoclonal light chain.

Background Fenfluramine hydrochloride was withdrawn from the market in September 1997 after reports of heart valve abnormalities in patients who used it. The prevalence of echocardiographic abnormalities and the clinical cardiovascular status of patients who received fenfluramine monotherapy remains uncertain. Methods A long-term, follow-up evaluation was undertaken in subjects who were randomly assigned to receive either fenfluramine hydrochloride (60 mg daily) or placebo as part of a double-blind smoking cessation therapy study. Cardiovascular status was evaluated by echocardiography, medical history, and physical examination. Results From the group of 720 smokers who had originally participated in the smoking cessation therapy trial, 619 women were enrolled; data from 530 (276 in the fenfluramine group and 254 in the placebo group) were evaluable. No statistically significant differences were identified in the prevalence of aortic or mitral regurgitation by Food and Drug Administration criteria or by grade, aortic or mitral valve leaflet mobility restriction or thickening, elevated pulmonary artery systolic pressure, or abnormal left ventricular ejection fraction. No significant differences were demonstrated in cardiovascular status by physical examination, and no serious cardiac events were noted among fenfluramine-treated subjects. Conclusion There was no evidence of drug-related heart disease up to 4.9 years after anorexigen therapy in subjects who were randomly assigned to receive fenfluramine at the recommended dose for up to 3 months.

We review the incidence of embolic events following cardioversion of atrial fibrillation, as well as the literature that forms the basis for the current strategy of anticoagulation before, and following, cardioversion to reduce the risk of post-cardioversion embolism. We evaluate a new strategy that uses transesophageal echocardiography to identify patients in atrial fibrillation without atrial thrombi who may be safely cardioverted without preceding anticoagulation and we also address the embolic event and anticoagulation issues in patients with atrial flutter. Cardioversion of atrial fibrillation to sinus rhythm is associated with a small but significant risk of thromboembolic events (average incidence, 1.5%; range, 0% to 7%). Anticoagulating these patients before cardioversion appears to significantly reduce this risk, and because of the delay in return of atrial contraction, anticoagulation should be continued for several weeks following cardioversion. The current guidelines for anticoagulating patients in atrial fibrillation who are to be cardioverted is based primarily on clinical observations, numerous uncontrolled case series, two retrospective trials, and one prospective nonrandomized controlled trial. Anticoagulation for 3 weeks before cardioversion followed by 4 weeks of anticoagulation after cardioversion is a theoretically sound and effective approach to reduce the risk of thromboembolic events. The use of transesophageal echocardiography to rule out thrombus and thus identify low-risk patients who may undergo cardioversion without preceding anticoagulation has been supported by several small studies that successfully used this strategy. However, the demonstration of a postcardioversion atrial and atrial appendage "stunning" suggests that anticoagulation needs to be given at the time of, and following, cardioversion. While promising, this transesophageal echocardiography—guided strategy for cardioversion of patients in atrial fibrillation requires more rigorous study before its routine use can be recommended. The current management of pure atrial flutter requires no anticoagulation before cardioversion; however, several clinical observations suggest theoretical risks for embolic events in these patients, thus further investigation of this strategy may be warranted. (Arch Intern Med. 1995;155:1353-1360)