R A O'rourke | PubMed Health

PubMed1977

Interventricular septal motion and left ventricular function after coronary bypass surgery: evaluation with echocardiography and radionuclide angiography.

To evaluate interventricular septal motion and left ventricular function after coronary bypass graft surgery, 40 patients were studied early postoperatively and serially for up to 16 months with echocardiography and radionuclide angiography. Early after operation mean left septal excursion decreased significantly from 4.6 +/- 0.4 (standard error) to 0.8 +/- 0.6 mm (P less than 0.001), and left septal motion was abnormal in 23 of the 40 patients. Mean right septal excursion reversed from 2.1 +/- 0.5 to -2.1 +/- 0.5 mm early after operation in the 22 patients in whom these measurements could be made, and 15 patients showed paradoxical right septal excursion. At a mean of 4 months after operation, only 7 of 35 patients followed up had abnormal left septal motion, and mean left septal excursion had returned toward normal (3.6 +/- 0.7 mm); mean right septal excursion remained reversed (--1.1 +/- 0.7 mm), and 6 of the 14 patients followed up had paradoxical motion. In the 22 patients whose wall thickness could be measured, mean septal thickening during systole decreased significantly from 35 +/- 4 to 21 +/- 3 percent early after operation (P less than 0.01). During late follow-up septal thickening returned toward normal (32 +/- 4 percent). Mean normalized posterior wall velocity increased significantly after operation from 0.76 +/- 0.03 to 1.01 +/- 0.05 sec-1 (P less than 0.001), but posterior wall thickening remained unchanged. Left ventricular end-diastolic dimension and the radionuclide-determined left ventricular ejection fraction were unchanged postoperatively. It is concluded that (1) echocardiographically detected abnormal septal movement is frequent early after coronary bypass graft operation; (2) both decreased myocardial contraction in the septum and increased anterior movement of the whole heart contribute to this abnormality; (3) the abnormalities in septal movement decrease during late follow-up in many patients but persist in some patients; and (4) posterior wall function tends to increase early after operation and therefore overall left ventricular function remains normal.

Adult↗

PubMed1977

Angina pectoris: an overview.

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Angina Pectoris↗

PubMedDate not supplied

The systolic click-murmur syndrome: clinical recognition and management.

The midsystolic click-late systolic murmur syndrome is a complex entity with variable manifestations that involves a primary process causing myxomatous degeneration of the mitral valve leaflet(s) and subsequent systolic mitral valve leaflet prolapse. Other cardiac diseases may cause mitral valve prolapse and regurgitation associated with a midsystolic click that mimics this primary syndrome. The prolapsing mitral valve leaflet(s) syndrome occasionally may be familial. Most patients are asymptomatic but some complain of chest pain, palpitation, dyspnea or fatigue. Prolapsing mitral valve leaflet(s) can be distinguished from other causes of systolic clicks and mitral regurgitation murmurs by the characteristic movement of the clikmurmur complex in systole with various hemodynamic interventions. The clinical diagnosis usually can be confirmed by echocardiography, which demonstrates the abnormally prolapsdrome usually is minimal but can be progressive and lead to the need for prosthetic valve replacement. Most symptomatic patients can be managed medically but some require cardiac catheterization to evaluate the possibility of coexistent coronary artery disease, to assess the degree of mitral regurgitation and to evaluate other associated cardiac lesions. All patients with this syndrome should receive antibiotic prophylaxis prior to any surgical or dental procedures. Those patients suspected of having arrhythmias should be evaluated by continuous ambulatory ECG monitoring and dangerous arrhythmias probably should be treated. The prognosis usually is excellent, but sudden death and rapidly progressive mitral regurgitation due to ruptured chordae tendineae have been reported. Although more than a decade has elapsed since the midsystolic click-late systolic murmur syndrome was first recognized, much remains to be learned about this common but complex clinical entity.

Adolescent↗