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A 72-year-old woman was admitted to our department for further investigation of a heart defect noted in transthoracic echocardiography performed in a district hospital. The patient complained of palpitations and moderately limited physical activity. On ECG, atrial fibrillation was recorded with a well-controlled ventricular rate. The chest x-ray demonstrated an enlarged heart and signs of moderate pulmonary congestion. The transthoracic echocardiography showed gross enlargement of the left atrium and its division into 2 compartments …

We read with interest the article by Zipes on TASERs1 that has received lay press coverage, with many news headlines and internet blogs reporting, perhaps erroneously, that the study’s findings reflect the position of the American Heart Association. This article describes 8 cases to support an opinion that TASERs can cause cardiac dysrhythmias and sudden death. However, we disagree with this conclusion, because there are a number of details of the cases that require further discussion. The Methods section states all subjects “were previously clinically healthy males;” however, criteria for “clinically healthy” were not defined. In fact, the table shows that all but one had a significantly enlarged heart or evidence of actual heart disease. When the reported heart weights were compared with the Mayo Clinic nomogram compiled by Kitzman et al,2 it was evident that all but patient No. 3 had mean heart weights greater than the …

Case presentation : A 73-year-old female smoker with a history of hypertension presents to the emergency room with dyspnea on exertion for 2 weeks, now progressing to shortness of breath at rest for 1 day. She has no angina, but has 2-pillow orthopnea and possible paroxysmal nocturnal dyspnea. On examination, blood pressure is 180/96 mm Hg, heart rate is 95 beats per minute and regular, and she is afebrile. Jugular venous pressure is 11 cm, and there are rales in the lower third of both lung fields. On cardiac auscultation there is an S4, but no S3 or murmur. On chest radiography, emphysematous changes are present, and there are patchy bilateral infiltrates consistent with pulmonary edema or pneumonia. Heart size is mildly increased. Is she suffering from congestive heart failure, and if so, why? What are the best management options acutely and after hospital discharge? Congestive heart failure (CHF) is one of the most common reasons for hospital admission in the United States. The syndrome usually evokes images of an enlarged heart with reduced systolic function. However, perhaps 50% of patients with CHF have normal or only minimally impaired systolic dysfunction and are diagnosed with diastolic heart failure (D-CHF) by exclusion.1–4 Rather than define D-CHF by what it is not (that is, CHF without systolic dysfunction), we regard D-CHF as CHF due to increased resistance to diastolic filling of part or all of the heart. Causes of D-CHF so defined are listed in Table 1; this review will focus on the myocardial causes.5,6 View this table: TABLE 1. Causes of Diastolic Congestive Heart Failure Depending on the cohort studied and the exact definition, the prevalence of D-CHF increases with age and is higher in women than men. Hypertension and left ventricular hypertrophy (LVH) are common. Compared with classic systolic CHF …

A65-year-old woman complained of nocturnal dyspnea, a period of stabbing pain between the shoulder blades, and swollen ankles that had persisted for 3 days. Physical examination revealed an irregular heart rate of 120 bpm; a blood pressure of 140/90 mm Hg in both arms; basal crepitations over both lungs; a grade 3/6 diastolic murmur maximal at the left sternal border; no abnormalities of the abdominal region; normal pulses of the radial, femoral, and carotid arteries; and ankle edema. An ECG showed atrial flutter with variable ventricular response and normal QRS-T complexes. Complete blood cell count, renal and hepatic function tests, and serological studies gave normal results. Chest radiograph showed an enlarged heart, an elongated aorta, normal lungs, and thoracic kyphosis. Transthoracic …

A 70-year-old man was referred for recent-onset angina. The ECG showed a right-axis deviation and signs of an old anterior infarction with loss of R waves in leads V1 through V5. Chest radiograph demonstrated a markedly enlarged heart, which was shifted to the left side with discrete signs of pulmonary congestion. Transthoracic echocardiography, which was limited by poor imaging quality, revealed a normal left ventricular cavity with reduced ejection fraction (40%) due to hypokinesia of the anterior wall. Coronary angiography showed the dominant RCA to originate from the left sinus of Valsalva. It coursed between the aorta and the pulmonary artery to the right (Figs …

The patient was a 31-year-old man with a past history of polycythemia vera, “enlarged heart” (1992), transient ischemic attack (1995), and decompensated heart failure (1997). He was referred for evaluation and management of suspected …

Rupture of a sinus of Valsalva aneurysm into the right ventricle produces a dramatic clinical syndrome characterized by a rapid and relentlessly unfavorable course. Early diagnosis is essential for surgical repair before an irreversible stage is reached. Cardiac catheterization and retrograde aortography confirmed the diagnosis in the case reported. With the aid of temporary circulatory occlusion, the fistula was demonstrated by contrast material injected via an aortic catheter. Although the fistula and the accompanying ventricular septal defect were closed at open-heart surgery, the markedly enlarged heart could not resume its function.

A series of investigations on the determinants of myocardial oxygen consumption were reviewed and their relevance to the survival and function of ischemic tissue in the presence of coronary occlusion pointed out. Tension development, contractile state of the myocardium, and heart rate are the most important factors influencing cardiac oxygen consumption, and drugs commonly used in the treatment of patients with acute myocardial infarction appear to influence oxygen consumption by acting upon these three determinants. Thus, digitalis glycosides and sympathomimetic agents tend to increase myocardial oxygen requirements, since they improve the heart's inotropic state. However, this influence may be offset in the enlarged heart in which end-diastolic volume and tension are reduced. Agents which depress the heart exert the opposite effect. Electrocardiographic changes reflecting myocardial ischemia are intensified when isoproterenol is administered following coronary ligation. Synchronized arterial counterpulsation reduces myocardial tension development and therefore oxygen consumption. An augmentation of myocardial oxygen needs in the presence of coronary occlusion may be expected to increase the size of the necrotic zone and to impair the function of the ischemic zone, while a reduction of oxygen consumption may be expected to exert the opposite effect.

Clinical and hemodynamic observations are reported in 13 patients who demonstrated a distinct pathophysiologic form of compressive pericardial disease characterized by effusion into a free pericardial space associated with constriction of the heart by the visceral pericardium. The pericardial disease was idiopathic (nine patients) or subsequent to radiotherapy (four patients), with a maximal duration of symptoms of 16 months. Enlarged heart shadow, prominent paradoxical pulse, predominant systolic dip in the venous pressure pulse, and absence of atrial fibrillation were features that tended to distinguish the effusive-constrictive cases from those with noneffusive chronic constrictive pericarditis. The value of pressure measurements during combined cardiac catheterization and pericardiocentesis is emphasized in the differentiation of effusive-constrictive pericarditis from cardiac tamponade without constriction. Four patients were observed to progress through an effusive-constrictive phase to noneffusive constrictive pericarditis. Corticosteroids, pericardiocentesis, and other medical therapy produced some benefit but did not relieve constriction. The results of surgery were generally satisfactory.

A review was made of the case histories and autopsy reports of 30 patients with systemic lupus erythematosus who had clinical cardiovascular involvement. The presence of an enlarged heart or of gallop rhythm strongly suggests myocardial involvement, but the electrocardiogram is not specific. Signs and symptoms referable to the heart are unusual as a first manifestation of systemic lupus erythematosus, and in patients receiving suppressive chemotherapy they do not further worsen the prognosis. Systolic murmurs cannot be interpreted as conclusive evidence of Libman-Sacks valvulitis.