We conclude that excessive ventricular hypertrophy, manifested as a markedly increased relative wall thickness, is associated with a significantly increased risk of postoperative mortality after aortic valve replacement for aortic stenosis.
Background. We examined the clinical and echocardiographic characteristics of patients undergoing aortic valve replacement for aortic stenosis whose continuous wave Doppler studies showed abnormal intracavitary flow acceleration.Methods and Resuls. The clinical and Doppler echocardiographic records of 53 consecutive patients undergoing aortic valve replacement for aortic stenosis were reviewed. Doppler echocardiography was performed at a mean of 6.6 days (range, 0-22 days) after surgery. Thirteen patients (group 1) had a dagger-shaped high-velocity systolic flow signal indicative of abnormal intracavitary flow acceleration on their postoperative Doppler study; group 2 comprised 40 aortic stenosis patients who underwent aortic valve replacement but had no postoperative evidence of abnormal intracavitary flow acceleration. Group 1 postoperative abnormal intracavitary flow velocities ranged from 1.8 to 6.8 m/sec (mean, 4.9±0.9 m/sec): Resulting dynamic gradients ranged from 10 to 184 mm Hg (mean, 104.6±32 mm Hg). Compared with group 2, group 1 patients had a distinctive ventricular geometry with more-pronounced hypertrophy, smaller cavities, and higher ejection fraction. Systolic anterior motion of the mitral valve did not accompany abnormal intracavitary flow acceleration in any patient. Six of 13 group 1 patients suflered postoperative hemodynamic compromise characterized by severe hypotension despite adequate pulmonary capillary wedge pressures; group 1 postoperative mortality was significantly greater than that seen in group 2 patients (38% versus 12%, p<0.05).Conclsions. Abnormal intracavitary flow acceleration after aortic valve replacement for severe aortic stenosis is associated with a distinctive ventricular geometry and supernormal systolic function but not systolic anterior motion of the mitral valve. Such flow acceleration appears to be a marker for increased postoperative morbidity and mortality. Preoperative and postoperative Doppler echocardiography may be useful in risk stratification and guiding therapy. (Circulation 1992;86:926-936)
To date, application of laser angioplasty in acute myocardial infarction (MI) has not been reported. In nine patients with acute myocardial infarction complicated by continuous or recurrent severe ischemia and chest pain, a mid-infrared, solid-state, pulse-wave holmium/thulium:YAG coronary laser was applied. In six of these patients the laser was specifically utilized for the purpose of coronary thrombolysis. In each case a guidewire was placed across the stenosis and a multifiber laser catheter was utilized, emitting 250-600 mJ/pulse at 5 Hz, followed by adjunctive balloon angioplasty. Laser success (defined as ability to cross the lesion, reduction of > or = 20% in stenosis and thrombolysis when a thrombus is present) was achieved in all patients. Final angiograms revealed residual stenosis < or = 30%, adequate thrombolysis and no major complication (MI, perforation, emergency CABGS, CVA, death) in each patient. Clinically, all nine patients improved, survived the acute infarction and were discharged. This initial clinical experience demonstrates the feasibility and safety of holmium/thulium:YAG laser application in thrombolysis and plaque ablation in selected patients who experience acute myocardial infarction complicated by prolonged or recurrent ischemia and chest pain.
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