Percutaneous transluminal coronary angioplasty of one vessel for refractory unstable angina pectoris: efficacy in single and multivessel disease.

Forty patients with unstable angina refractory to medical treatment had one vessel percutaneous transluminal angioplasty to the most stenotic lesion in a major coronary artery. The procedure was successful in 35 patients, and the remaining five patients underwent emergency coronary artery bypass graft surgery. The initial success rate (84%) for the 16 patients with single or the 19 patients with multivessel disease (90%) was similar. At early follow up (average nine days) all patients with successful angioplasty remained symptomatically improved; 10 patients (83%) with single and 10 patients (63%) with multivessel disease had negative treadmill stress tests. Five of six cardiac events occurred within the intermediate (average 11 months) follow up period; two patients had recurrent refractory unstable angina, two had angioplasty for progression of disease in a vessel not previously treated by angioplasty, and one had bypass graft surgery. During late (average 26 months) follow up one patient had a non-fatal myocardial infarction while seven patients (58%) with single vessel disease and nine patients (75%) with multivessel disease had negative stress tests; 29 of 40 patients showed long term improvement.

Intracoronary prostaglandin E1 plus streptokinase in acute myocardial infarction.

Fourteen patients with acute myocardial infarction (duration of chest pain 5 +/- 2 hours) received intracoronary infusion of prostaglandin E1 (PGE1) and streptokinase. Intracoronary PGE1 was followed by intracoronary streptokinase in 10 patients (group A), with successful recanalization in all patients. Of 4 patients in whom recanalization failed with intracoronary streptokinase given first (group B), 2 had successful recanalization after addition of intracoronary PGE1. Immediately after successful recanalization, left ventricular ejection fraction increased from 50 +/- 9% to 62 +/- 10% (p less than 0.0008), left ventricular end-diastolic pressure decreased from 20 +/- 10 to 16 +/- 10 mm Hg (p less than 0.05) and stroke volume index increased from 34 +/- 10 to 44 +/- 12 ml/m2 (p less than 0.02). Infarct segment shortening improved from 9 +/- 5 to 18 +/- 4% (p less than 0.0002). Transient hypotension in 1 patient was the only complication. Follow-up catheterization in recanalized patients at 2 to 10 days showed maintained improvement in left ventricular global and infarct segment function. Reocclusion occurred in 1 patient. Thus, intracoronary infusion of PGE1 was effective in establishing reperfusion in all patients when followed by streptokinase and was associated with immediately improved left ventricular global and regional function. PGE1 deserves further evaluation in acute myocardial infarction.

Cardiopulmonary hemodynamics in perinephritic hypertensive dogs: effect of intravenous volume load.

To investigate the role of decreased venous distensibility in the regulation of cardiac output, cardiopulmonary hemodynamic measurements were performed at rest and after a volume load (6% dextran in saline, 12 ml/kg iv) in 18 awake dogs with chronic one-kidney, one-wrapped hypertension and 9 normotensive control dogs. The distribution of blood volume between the peripheral and cardiopulmonary vascular beds and the increase in cardiac output after volume load in the two groups of dogs were the same. There was no echocardiographic evidence of left ventricular dysfunction (shortening fraction) in hypertensive dogs. The rise of heart rate after volume load in hypertensive dogs, 17 +/- 3 beats/min (mean +/- SE), was attenuated compared to that of control dogs, 38 +/- 4 (p less than 0.001). Compared to values in normotensive dogs, the in vitro left atrial pressure-volume curves of hypertensive dogs were shifted in the direction of the pressure axis (p less than 0.02). The findings do not provide a role for decreased venous distensibility in the regulation of cardiac output in chronic renal hypertension. Decreased distensibility of the left atrium may play a role in the pathogenesis of the attenuated Bainbridge effect in hypertensive dogs.

Echocardiographic evidence for increased cardiac performance during early renal hypertension in dogs.

Cardiac function early (less than 4 weeks) in the course of experimental renal hypertension was investigated. In 11 male mongrel dogs, one kidney was wrapped in silk to produce two-kidney, one-wrapped hypertension. Two weeks later, the contralateral kidney was removed. Five sham-wrapped and then contralaterally-nephrectomized dogs served as controls. M-mode left ventricular (LV) echocardiograms were recorded twice weekly in all dogs for 4 weeks before and for 2 weeks after wrapping (or sham-wrapping) and for 4 weeks after nephrectomy. In the 11 hypertensive dogs, mean arterial pressure (MAP) rose from 127 mm Hg (mean) to 143 two weeks after wrapping (p less than 0.05) and to 185 two weeks after nephrectomy (p less than 0.001). The fractional shortening of the left ventricle (% delta D) of hypertensive dogs was increased (9% maximum, mean, p less than 0.01) for 2 weeks after wrapping and for one week after nephrectomy. Two weeks after wrapping, LV end-systolic wall stress calculated from femoral artery peak systolic pressure, end-systolic dimension and wall thickness was unchanged, suggesting that increased myocardial contractility accounted for the findings. In normotensive control dogs, there were no echocardiographic changes during the study.

Short-term systemic hemodynamic adaptation to beta-adrenergic inhibition with atenolol in hypertensive patients.

Early systemic hemodynamic adjustments to antihypertensive therapy with the cardioselective beta inhibitor, atenolol, were investigated in 12 hospitalized men, mean age 52 years, with uncomplicated mild-to-moderate essential hypertension. Twice daily measurements of cardiac output (CO) by CO2 rebreathing, blood pressure by cuff, and heart rate were performed in all subjects for 3 days before and 5 days after initiation of oral atenolol therapy (50 or 100 mg daily). Cardiac output by CO2 rebreathing was checked with dye dilution just before, and 4 hours and 4 days after the start of therapy. Plasma volume (radioiodinated albumin) was measured before therapy and on Day 5 of therapy. The CO results obtained with the two methods were not significantly different (r = 0.88, p less than 0.01, n = 12). A reduction in heart rate, 18 +/- 2 beats/min (mean +/- SE), occurred in all patients while taking atenolol. By 4 hours after the first dose of atenolol, CO fell from 5.49 +/- 0./30 to 4.24 +/- 0.21 liters/min (p less than 0.01), while the control mean arterial pressure (MAP) of 108 +/- 4 mm Hg was not significantly changed, 110 +/- 4 mm Hg. At 24 hours, CO returned near baseline (5.10 +/- 0.21 liters/min) but MAP was reduced (95 +/- 3 mm Hg, p less than 0.001) and remained so thereafter. CO remained at baseline at 48 hours (5.50 +/- 0.29 liters/min) but fell again (p less than 0.01) to 4.81 +/- 0.11 on Day 4 and to 4.68 +/- 0.25 liters/min on Day 5 of atenolol therapy. Plasma volume, 3110 +/- 100 ml before therapy, was reduced to 2850 +/- 100 by Day 5 of atenolol therapy (p less than 0.01). The findings indicate a delayed onset of the antihypertensive action of atenolol. The transient return to baseline of CO on Day 2 and 3 of atenolol therapy suggests a reverse autoregulatory adjustment to the initial fall in CO.