Mitral valve regurgitation (MR) is a frequent Doppler echocardiographic finding in patients after acute myocardial infarction (AMI) and an independent predictor of long-term cardiovascular mortality. Reported risk factors include advanced age, prior myocardial infarction, infarct extension, and recurrent ischemia. During the early phase of AMI, transient ischemic MR is common and rarely causes hemodynamic compromise. However, when several chordae tendineae or a papillary muscle ruptures, acute left atrial and ventricular volume overload ensues, leading to abrupt hemodynamic deterioration with cardiogenic shock. Auscultation may be unrevealing due to decreased turbulence. Hence, the importance of a high index of suspicion for acute MR in any patient with acute pulmonary edema in the setting of AMI, especially if left ventricular systolic function is well preserved. Later, ventricular remodeling may lead to MR through annular dilatation or papillary muscle migration with malcoaptation of the leaflets. The widespread availability, ease of use and non-invasive nature of Doppler echocardiography have made it the standard diagnostic tool for detecting MR. Mechanical reperfusion of the infarct-related artery seems to be superior to fibrinolysis in decreasing its incidence acutely and in the long run. Nevertheless, when acute severe MR occurs, unless rapidly diagnosed and treated, this dreaded complication is associated with high morbidity and mortality. Prompt surgical intervention after hemodynamic stabilization is essential to ensure a good short-term and long-term prognosis. This review discusses the incidence, long-term prognosis, associated risk factors, complex pathophysiology, time of occurrence, clinical manifestations, diagnosis, and management of patients with MR after AMI.

Ventricular free wall rupture remains a dreaded complication of acute myocardial infarction. A dramatic fatal presentation is not universal and if recognized early, especially in its sub-acute form, a therapeutic intervention may be lifesaving. Changing trends in its natural history and the previously described pathological subtypes have emerged since the advent of thrombolysis. Although frequently unpredictable, certain clinical, echocardiographic and electrocardiographic signs should suggest the diagnosis. Moreover, knowledge of predisposing risk factors and a high index of suspicion are helpful in early recognition of this complication. In recent years, several different therapeutic approaches have been described including percutaneous seals and surgical mechanical closure of ventricular free wall rupture. In this review, we sought to highlight established and debatable aspects of this pathology to hopefully enhance prompt diagnosis and treatment by all clinicians caring for patients suffering acute myocardial infarction.

Color M-mode flow propagation velocity seems to be a preload-independent measure of diastolic function in chronic hemodialysis patients in whom isolated diastolic dysfunction appears prevalent.

Summary: This paper reports on two cases of large volume pericardiocentesis followed by transient severe acute left ventricular (LV) systolic failure in the absence of any prior history of LV dysfunction. Acute LV volume overload due to interventricular volume mismatch is believed by most authors to be the cause for this phenomenon. Another plausible physiopathologic explanation is the acute increase in "wall stress" (Laplace's law) due to acute distention of the cardiac chambers secondary to a sudden increase in venous return at high filling pressures, combined with a "vacuum" effect of the evacuated pericardial space. A 36-year-old woman with severe rheumatic mitral stenosis and tricuspid insufficiency, pulmonary hypertension, and chronic atrial fibrillation underwent mitral valve replacement and surgical repair of the tricuspid valve at an outside hospital 2 months before the present admission. She had been taking digoxin, warfarin, and furosemide. During the week preceding the index admission she had developed progressive dyspnea. On admission, transthoracic echocardiography (TTE) showed a large pericardial effusion with partial compression of the right heart, right ventricular (RV) dilatation, moderate to severe tricuspid regurgitation (with severely increased estimated RV systolic pressure) and normal left ventricular (LV) systolic function. The pressure gradient across the prosthetic mitral valve was within expected limits. Her electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular response and no electrical alternans. Because of prolonged prothrombin time due to coumadin therapy and lack of clinical signs of tamponade, conservative approach with steroids was instituted first. However, dyspnea worsened, and 3 days later the patient underwent pericardiocentesis under echocardiographic guidance, with evacuation of 1070 ml of serous fluid. During the following hours, the patient's condition deteriorated. She became tachypneic, her heart rate increased, and blood pressure decreased. On the next morning she developed overt cardiogenic shock. Repeat TTE showed severe LV dysfunction with regional wall motion abnormalities without pericardial effusion. Her ECG was unchanged from admission. Ultimately, the pericardial fluid was consistent with an exsudate with increased proteins and inflammatory cells consistent with postpericardiectomy pericarditis. Because of the presence of regional wall abnormalities, the patient underwent urgent coronary angiography that demonstrated angiographically normal coronary arteries. An intra-aortic balloon pump was inserted, the patient received high-dose inotropic support with dobutamine and diuretics, and her clinical condition improved. After inotropic support was discontinued, repeat TTE 4 days later showed significant improvement in LV function. Two weeks later she was discharged from the hospital on beta blockers, digoxin, warfarin, and furosemide. At discharge, TTE showed normal LV function without regional wall motion abnormalities and with normally functi...

SummaryBackground: Rapid screening of cardiac patients with a hand-held ultrasound imager (SonoHeart ™ [SH]) could provide valuable clinical information.Hypothesis: Whether the use of this device yields additional information to a carefully conducted physical examination and comparable findings to those of conventional two-dimensional echocardiography (2-D) during inpatient rounds is not well established and is the subject of this study.Methods: In all, 100 consecutive telemetry patients underwent rapid screening with 2-D and color Doppler SH during inpatient rounds. SonoHeart findings were compared with results from conventional 2-D and physical examination conducted by an attending cardiologist.Results: All patients had interpretable images. Mean scanning time with SH was 5.0 ± 1.2 min; 2-D and SH findings were comparable. The parameters studied included chamber sizes, left ventricular (LV) systolic function, presence of LV hypertrophy (LVH), wall motion abnormalities (WMA), pericardial effusion (PE), and valvular regurgitations. Mild to moderate valvular regurgitation and LV systolic dysfunction were reliably diagnosed by SH in a number of patients whose symptoms were unrelated to the abnormalities detected.