We conclude that the LAA has a characteristic pattern of emptying in sinus rhythm. LAA thrombus formation in sinus rhythm and atrial fibrillation is associated with both poor LAA contraction and LAA dilation.

ED is extremely common in men with chronic coronary artery disease (affecting approximately 75%) yet most cardiologists do not ask about it. The SHIM is a useful, quick and inexpensive tool for discussion and diagnosis of ED in this population. Although it is well established that cardiovascular risk factors are associated with erectile dysfunction, once it is present there is mixed information on whether treating the risk factors will treat the ED. Problems appear to be that lifestyle modification in midlife may simply be too late to effect a change, and some antihypertensive and lipid lowering drugs may actually exacerbate ED. Oral therapy for ED, namely the PDE5 inhibitors, is effective and safe in most cardiac and hypertensive patients. Organic nitrates such as nitroglycerin remain a contraindication to the concomitant use of these drugs. Guidelines for treatment of ED in the cardiac patient issued by the American College of Cardiology/American Heart Association and Princeton Guidelines may be useful in the approach to the cardiac patient with ED.

Although electrocardiographic (ECG) abnormalities and autopsy evidence of myocardial necrosis are associated with subarachnoid hemorrhage, their relation to in vivo measures of left ventricular function in this condition has not been established. Thirteen patients with subarachnoid hemorrhage and no prior history of heart disease were studied by two-dimensional echocardiography, performed initially 10 to 48 h (mean 18) after admission and serially for less than or equal to 14 days. Serum creatine kinase (total and myocardial isoenzyme) was determined 5 times over the first 48 h; ECGs were performed daily. Neurologic state was assessed with the use of a standard grading system. Four patients (Group I) exhibited left ventricular wall motion abnormalities in one to eight segments. In two of these patients there was also left ventricular apical mural thrombus that embolized in one patient, leading to further neurologic deterioration. The initial creatine kinase myocardial isoenzyme was higher in Group I than in Group II (patients without wall motion abnormalities) (10.3 versus 2.1 U/liter, p less than 0.001), initial heart rate was higher (91 versus 61 beats/min, p less than 0.01), neurologic grade was higher (2.5 to 4.5 versus 1 to 2, p less than 0.001) and inverted T waves were more common (4 of 4 versus 1 of 9). Three of the four patients in Group I died; two of the three underwent autopsy and were found to have no significant coronary artery disease. No other patients died.(ABSTRACT TRUNCATED AT 250 WORDS)

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Femoral vein contrast delivery significantly enhances the ability of precordial contrast echocardiography to diagnose patent foramen ovale. Physiologic patency of the foramen ovale is more common (prevalence 33%) than previously documented.

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We performed simultaneous echocardiographic and hemodynamic studies in 11 patients with muscular subaortic stenosis to determine whether systolic anterior motion (SAM) of the anterior mitral leaflet and the pressure gradient are related quantitatively. SAM without septal contact was associated with either no gradient or a small impulse gradient of less than 10 mm Hg. SAM with septal contact was always associated with a pressure gradient of more than 10 mm Hg. The size of the pressure gradient correlated inversely with the time periods: (1) onset of SAM-septal contact (r = .79, p less than .001) and (2) onset of aortic ejection to onset of SAM-septal contact (r = -.89, p less than .001). Size also correlated directly with the time period: (3) duration of SAM-septal contact (r = .80, p less than .001). Thus when the time from the onset of SAM to the onset of SAM-septal contact was long, SAM-septal contact developed late in systole, the duration of SAM-septal contact was brief and the pressure gradient was low. When SAM-septal contact developed in early systole, the duration of SAM-septal contact was long and the pressure gradient was high. With the index of time period (3) divided by time period (1), a regression equation was devised to predict the size of the pressure gradient (pressure gradient [mm Hg] = 25 [ratio] + 25; r = .90, p less than .001; SE +/- 15 mm Hg). The echocardiographic time period index was validated prospectively in nine other patients and the significant correlation with the hemodynamically determined gradient persisted (r = .89, p less than .01). We conclude that SAM and the pressure gradient are related quantitatively in muscular subaortic stenosis. These observations have implications regarding the mechanism and significance of the pressure gradient in muscular subaortic stenosis.