Repeat coronary angioplasty: efficacy of a third angioplasty for a second restenosis.

To determine the efficacy of repeat percutaneous transluminal coronary angioplasty, 74 patients were studied who underwent a third angioplasty for a second restenosis of one coronary artery segment. The procedure was successful in 93% of patients. Procedural complications included emergency bypass surgery (three patients) and in-hospital death (two patients). At late follow-up (mean 18 months, range 7 to 49), 30 patients (43%) had a third restenosis treated with either a fourth angioplasty (16 patients), coronary bypass surgery (11 patients) or medical management (1 patient). Thirty-nine patients (57%) had no restenosis on the basis of follow-up angiography or absence of symptoms previously attributed to restenosis. Factors associated with a third restenosis included a shorter time interval (less than 3 months) between previous angioplasty procedures and dilation of the left anterior descending coronary artery. Among the 16 patients undergoing a fourth angioplasty for a third restenosis, the procedural success rate was 94%. One patient required emergency bypass surgery. At late follow-up (mean 16 months, range 7 to 38), eight patients (53%) had a fourth restenosis treated with either a fifth angioplasty (one patient), bypass surgery (five patients) or medical management (two patients). Considering all 74 patients undergoing a third angioplasty for a second restenosis, 27% had bypass surgery, 5% died, 4% were managed medically and 64% were free of angina at late follow-up after either a third, fourth or fifth angioplasty. Restenosis rates after a third or fourth angioplasty procedure for recurrent restenosis are higher than those for the initial procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of endothelial and inducible nitric oxide synthases inhibition on circulatory function in rats after myocardial infarction.

OBJECTIVES: To examine the relative roles of eNOS and iNOS (endothelial and inducible nitric oxide synthases) on basal and beta-adrenergic receptor (beta-AR)-stimulated arterial hemodynamic responses after myocardial infarction (MI). METHODS: Left ventricular (LV) pressures and steady-state and pulsatile arterial hemodynamics were measured at baseline, and after acute NOS inhibition with either NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/kg) or iNOS inhibition with aminoguanidine (AG, 75 mg/kg) in sham-operated and MI Sprague-Dawley rats. RESULTS: In sham rats, L-NAME decreased (P < 0.05) peak positive LV dP/dt and aortic blood velocity by 19% and 53%, respectively, and increased (P < 0.05) mean arterial pressure (MAP); systemic vascular resistance, and LV end-diastolic pressure (EDP) by 20, 189 and 89%, respectively. The frequency-dependent components of hemodynamics including aortic input impedance modulus, characteristic impedance, and phase shift were increased (P < 0.05) with L-NAME, while pulsatile power was decreased (P < 0.05). AG increased (P < 0.05) aortic input impedance modulus and characteristic impedance but had no effect on any other hemodynamic variable. In MI rats, L-NAME decreased (P < 0.05) LV dP/dt and aortic blood velocity by 22 and 55%, respectively, and increased (P < 0.05) SVR by 108%. There was no effect of L-NAME on MAP or LV EDP in MI rats. After MI, AG increased (P < 0.05) heart rate and LV dP/dt but had no effect on other LV or pulsatile hemodynamic variables. Compared to sham rats, heart rate, LV dP/dt, and blood velocity-isoproterenol dose responses were shifted downward (P < 0.05), while SVR-isoproterenol dose response was shifted upward (P < 0.05) in MI rats. In sham rats, L-NAME potentiated (P < 0.05, at > 10(-2) micrograms/kg) the isoproterenol-induced increase in LV dP/dt and aortic blood velocity, and potentiated (P < 0.05) the isoproterenol-induced decline in SVR. As expected, AG had no effects on isoproterenol-stimulated hemodynamics in sham rats. After MI, there was no effect of L-NAME or AG on isoproterenol-stimulated hemodynamics. CONCLUSIONS: (1) Circulatory and cardiac responses to inhibition of NO by L-NAME suggest that eNOS, but not iNOS, is the principal regulator of integrated arterial hemodynamic function in rats. (2) Both basal and beta-AR-stimulated NO regulation of hemodynamic are attenuated after MI. (3) The attenuation of arterial hemodynamic effects after isoproterenol is mediated, in part, by alterations in the beta-AR-activation of eNOS system after MI.

Vocal fold mucosal tears: maintaining a high clinical index of suspicion.

Vocal fold mucosal tears have been discussed in the literature rarely, although they are not uncommon clinically. Disruptions in the epithelium usually follow trauma that may result from voice abuse and/or misuse, coughing, and other causes. A high index of suspicion is necessary to avoid missing vocal fold mucosal tears, and strobovideolaryngoscopy is indispensable in making the diagnosis. A brief period of complete voice rest is the standard of care and appears to be helpful in avoiding adverse sequelae and advancing the healing process, but there are no scientific studies to confirm its efficacy. Mucosal tears may heal completely or may be followed by the development of vocal fold masses, scar, and permanent dysphonia.