Tumor of the heart diagnosed by magnetic resonance imaging.

A case of liposarcoma metastatic to the heart is presented. This is a very rare entity and only three prior case reports could be found. Magnetic resonance imaging was successfully used to visualize the tumor. These images compared favorably with a two-dimensional echocardiographic study and postmortem examination.

Relation of angina pectoris to coronary artery disease in aortic valve stenosis.

One hundred three patients with isolated, severe aortic stenosis (AS) were retrospectively analyzed to determine the relation of angina pectoris to angiographically significant coronary artery disease (CAD). All patients underwent coronary angiography regardless of the presence or absence of angina. Angina was significantly associated with CAD (p less than 0.002), with a sensitivity of 78% and a specificity of 53%. However, 25% of the patients without angina had angiographically significant CAD, and in these patients there was a 70% prevalence of 1-vessel disease. Patients with isolated, severe AS should undergo coronary angiography to identify coexistent CAD accurately. The absence of angina does not reliably exclude angiographically significant CAD.

Frequency of angiographically significant coronary arterial narrowing in mitral stenosis.

Ninety-six consecutive patients older than 40 years with severe mitral stenosis were retrospectively analyzed to determine the relation of angina pectoris (AP) and coexistent coronary artery disease (CAD). Of the 96 patients, 27 (28%) had angiographically significant CAD, 10 (37%) with AP and 17 (63%) without AP. Of the 96 patients, 21 had AP, 10 (48%) with angiographically significant CAD and 11 (52%) without (CAD). Of 75 patients without AP, 17 (23%) had angiographically significant CAD AP had a specificity of 84% and a sensitivity of 37% in its ability to detect significant CAD. The pulmonary artery systolic, diastolic and mean pressures and the pulmonary vascular resistance did not differ between patients with and those without AP (p greater than 0.05). It is concluded that coexistent CAD is commonly found in patients older than age 40 with severe MS, and is usually clinically silent.

Angina pectoris and coronary artery disease in isolated, severe aortic regurgitation.

Seventy-eight patients with isolated, severe aortic regurgitation (AR) were studied retrospectively to determine the prevalence of angiographically significant coronary artery disease (CAD) and its relation to angina pectoris (AP). Angiographically, significant CAD was present in 29 of 78 patients (37%), and 36 patients (46%) had AP. Twenty-one of 36 patients (58%) with AP and 8 of 42 patients (19%) without AP had angiographically significant CAD. AP as a predictor of significant CAD had a sensitivity of 73%, specificity of 69% and a risk ratio of 3:1. The predictive accuracy of detecting CAD in the absence of AP was 81%. The benefit from concomitant coronary artery bypass grafting at the time of aortic valve replacement for AR has not been clearly demonstrated; therefore, routine coronary angiography is still recommended for all AR patients older than 40 years undergoing aortic valve replacement.

Echocardiographic identification of intrapericardial fibrous strands in acute pericarditis with pericardial effusion.

In three cases of acute pericarditis with pericardial effusion, the presence of fibrous strands within the fluid-filled pericardial cavity was demonstrated by M-mode and cross-sectional echocardiography. Pericardiocentesis proved difficult in all three. No patient progressed to constrictive pericarditis.

Aortic dilatation resulting in chronic aortic regurgitation and complicated by aortic dissection in a patient with Turner's syndrome.

A patient with XO Turner's syndrome with a 12-year history of progressive aortic root dilatation resulting in chronic aortic regurgitation is presented. Her case is unique in that it occurred in the absence of coarctation of the aorta, bicuspid aortic valve, or hypertension. Idiopathic dilatation of the aorta may be an additional risk factor to the development of aortic dissection in the setting of Turner's syndrome.

Clinical and echocardiographic features of isolated severe pure mitral regurgitation.

Recent studies have shown that rheumatic heart disease is no longer the main cause of isolated severe pure mitral regurgitation. In this study, we evaluated various clinical and echocardiographic features found in the syndrome of mitral regurgitation. Our data is consistent with recent reports that mitral valve prolapse and coronary artery disease are now the predominant causes of mitral regurgitation and that rheumatic heart disease is a much less common etiology. In addition, our data suggest that clinical evaluation alone is usually very accurate in identifying the correct etiology. Various clinical and echocardiographic features found in the subsets of acute and chronic mitral regurgitation are described. Specifically, patients with acute mitral regurgitation were more likely to have echocardiographic evidence of segmental left ventricular dysfunction and flail mitral valve leaflet. In chronic mitral regurgitation, atrial fibrillation and left atrial dilatation were more commonly present. Echocardiography was found to be more useful in the detection of the complications of coronary artery disease rather than in identifying its presence. Patients with a New York Heart Association classification of IV and those with echocardiographic evidence of an increased left ventricular endsystolic dimension or left ventricular hypertrophy had a worse prognosis.

Persistent atrial quiescence in adult rheumatic heart disease.

The first adult patient with catheterization-proven isolated rheumatic heart disease who demonstrated the electrophysiologic findings of "persistent atrial quiescence" is described. Metabolic causes of transient atrial sequence were effectively excluded by clinical history and appropriate laboratory studies. Atrial quiescence may be the electrophysiologic expression of end-stage rheumatic atrial pathology seen only in cases of advanced, surgically uncorrected rheumatic mitral valve disease.

Cardiac manifestations of the antiphospholipid syndrome.

The antiphospholipid syndrome has been associated with multiple cardiac abnormalities. The earliest reports were of valvular disease, including verrucous endocarditis, as well as valvular thickening and insufficiency. Subsequently, antiphospholipid antibodies were implicated in coronary artery disease manifested by premature myocardial infarction and coronary artery bypass graft occlusion. In addition, there have been rare reports of intracardiac thrombi and diffuse cardiomyopathy in association with antiphospholipid antibodies. In this review, we discuss the nature and prevalence of the cardiac manifestations of the antiphospholipid antibody syndrome as well as some of the proposed pathophysiologic mechanisms. We also provide examples from our own experience. The expanding spectrum of cardiac disease associated with antiphospholipid antibodies suggests an important role for these antibodies in certain types of cardiac pathology.

Somatotype and idiopathic mitral valve prolapse.

Records from 18 subjects with angiographic idiopathic mitral valve prolapse, 28 subjects with merely exaggerated posterior mitral leaflet systolic bulging, and 100 subjects with normal hemodynamic and angiographic findings were compared with regard to age, sex, height, weight, ponderal index (height/3 square root weight), auscultatory and echocardiographic abnormalities. Chest x-ray films available for subjects with mitral valve prolapse were reviewed. The ponderal index of subjects with mitral valve prolapse (13.1 +/- 0.8) differed from that of subjects with merely exaggerated posterior mitral leaflet systolic bulging (12.6 +/- 0.7) (P less than 0.02) and from that of subjects without angiographic abnormality (12.3 +/- 0.8) (P less than 0.001). The three groups differed in ponderal index when equated statistically for age, height, weight, and sex (P less than 0.001). Among mitral valve prolapse patients, an asthenic habitus occurred independent of the presence of thoracic skeletal abnormalities.

Left atrial size, pressure, and V wave height in patients with isolated, severe, pure mitral regurgitation.

In recent years, some concepts regarding the etiology and hemodynamics present in the syndrome of mitral regurgitation have changed. Coronary artery disease and mitral valve prolapse have replaced rheumatic heart disease as the most frequent cause of mitral regurgitation. Hemodynamic studies have shown that tall V waves in the pulmonary capillary wedge tracings are neither specific nor sensitive in detecting the presence of mitral regurgitation. In this study, we evaluated the role of various clinical, echocardiographic, and hemodynamic findings with regard to left atrial (LA) size, pressure, and V wave height. We found that the mean pulmonary capillary wedge pressure (PCW) and V wave height for the subset of patients with acute mitral regurgitation (PCW = 24.1 +/- 10.9; V = 41.2 +/- 20.7 mm Hg) was similar to the subset with chronic mitral regurgitation (PCW = 17.9 +/- 7.5; V = 32.0 +/- 18.2 mm Hg). In addition, we found that there was a significant logarithmic relationship between the LA size and the duration of the mitral regurgitation (y = 1.404 [log X] + 3.948; R = 0.678; p less than 0.0005). Lastly, we found that LA size, compliance, regurgitant volume, and regurgitant valve orifice area all increase with time.

Clinical manifestations and therapy of Lactobacillus endocarditis: report of a case and review of the literature.

A case of Lactobacillus casei endocarditis that occurred on a Carpentier-Edwards porcine valve is reported. A review of the literature, which yielded 23 other reports of endocarditis due to this organism, suggests that Lactobacillus is a rare cause of endocarditis. Typically, it occurs in a patient with preexisting structural heart disease (20 of 24 [83%]) and often with some form of recent dental infection or manipulation (18 of 24 [75%]). Six (25%) of 24 patients died of this infection; however, only one (5%) of 19 who were treated with adequate antimicrobial therapy died. The response to antimicrobial therapy was better in the more recent cases. Of those 18 patients who completed a full course of therapy, seven (39%) experienced a relapse; five of these were cured of their infection with a second course of antimicrobial therapy, which usually included higher doses of intravenous penicillin. Our case represents the second reported case that required surgical intervention for cure. Embolic phenomena occurred in 10 (42%) of 24 cases. Various combinations of antibiotics have been successful in achieving cure; however, at present, high-dose penicillin (greater than 25 million units/day) in combination with an aminoglycoside for a period of six weeks appears to be the optimum therapy.

Resting and exercise hemodynamics in constrictive pericarditis and a case of cardiac amyloidosis mimicking constriction.

The resting and exercise hemodynamics in seven patients with pericardial constriction and in one patient with cardiac amyloidosis are described. Equalization of left and right heart diastolic filling pressures was observed in all cases, both at rest and during exercise. This hemodynamic response, although typical, should not be considered pathognomonic of pericardial constriction.

Viridans streptococcal endocarditis: clinical, microbiological, and echocardiographic correlations.

Infections caused by species within the viridans streptococci have been associated with different clinical characteristics. We studied 36 patients with viridans streptococcal endocarditis. Complications were seen in 10 (32%) of 31 patients with native valve endocarditis and four (80%) of five with prosthetic valve endocarditis and included death in two, valve replacement in six, persistent infection in three, emboli in two, and congestive heart failure in nine. Two-dimensional echocardiograms demonstrated vegetations in 26 (72%) of 36, flail mitral valves in seven, disruption of aortic valve prosthesis in one, and perivalvular abscesses in three (two Streptococcus sanguis I and one Streptococcus intermedius I). All twelve patients with native valve endocarditis who suffered complications had vegetations detected by two-dimensional echocardiography, whereas seven patients with native valve endocarditis without vegetations, as detected by two-dimensional echocardiography, had no complications (P = .03). We found no significant correlation between streptococcal species and clinical outcome. To confirm our identifications, we sent 16 identical viridans streptococcal endocarditis isolates to five institutions; only three of 16 were identified as the same species by all five institutions. We conclude that viridans streptococcal endocarditis can be associated with a virulent clinical course and that there is marked variability in species designations of individual strains by different laboratories.