Clot-selective coronary thrombolysis with low-dose synergistic combinations of single-chain urokinase-type plasminogen activator and recombinant tissue-type plasminogen activator. The Pro-Urokinase for Myocardial Infarction Study Group.

The effect of simultaneous infusions of low-dose recombinant tissue-type plasminogen activator (t-PA) and single-chain urokinase-type plasminogen activator (scu-PA, pro-urokinase) on coronary arterial thrombolysis was investigated in 23 patients treated within 6 hours (mean 2.6 +/- 1.1, range 1.2 to 5.9) of symptoms of an acute myocardial infarction. Infarct artery patency at 90 minutes was achieved in 16 (70%, 95% confidence limits of 0.47 to 0.87) of 23 patients after a 1-hour intravenous infusion of 20 and 16.3 mg of t-PA and scu-PA, respectively. At 90 minutes, the fibrinogen concentration decreased from 369 +/- 207 to 316 +/- 192 mg/dl (p = not significant), while plasminogen decreased to 69 +/- 24% (p = 0.001) and alpha-2-antiplasmin to 77 +/- 24% (p = 0.001) of pretreatment values. Although no bleeding requiring termination of drug infusion or transfusion occurred, 1 patient with cerebrovascular amyloidosis had a fatal intracerebral hemorrhage. These findings suggest that combination therapy may allow substantial reductions in total thrombolytic doses while still achieving effective fibrin-specific coronary thrombolysis.

Ranitidine-induced chest pain.

A 45-year-old woman with no history of heart disease twice experienced chest pain after consuming a dose of ranitidine. The chest pain, which lasted about one hour, was substernal, left of midline, dull, and pounding. H2-receptors are present in cardiovascular tissues. Although several studies have not noted an effect of ranitidine on cardiac indices there have been case reports indicating a cardiac effect. There are no reports of chest pain associated with H2-blocker ingestion; however, both bradycardia and hypotension (reported effects) might cause chest pain. A discussion of the possible mechanisms is presented.

A prevalent misconception regarding wide-complex tachycardias.

In response to a questionnaire, 59% of 196 physicians indicated that they were influenced by a patient's blood pressure and clinical status when attempting to distinguish ventricular tachycardia (VT) from paroxysmal supraventricular tachycardia with bundle-branch block. A sizable proportion of physicians are unaware that VT need not be associated with shock. More emphasis should be placed on making physicians aware that the differentiation of VT from paroxysmal supraventricular tachycardia should be based on electrocardiographic findings and not on the patient's blood pressure or clinical status.

The effects of coronary angioplasty and reperfusion on distribution of myocardial flow.

To assess the effects of angioplasty (PTCA) and intracoronary streptokinase (ICSK) on relative myocardial perfusion, we administered 99mTc-macroaggregated albumin (MAA) to the uninvolved coronary artery before successful PTCA in 33 patients and before successful infusion of ICSK in eight patients and of 111In-MAA into the same vessel after the intervention. In 10 patients who underwent PTCA, MAA was injected into the involved, instrumented coronary artery. Computer-processed images were acquired in registry and compared. Similar scintigraphic studies were performed in six control patients and in 11 in whom planned interventions were not performed or were unsuccessful. Distribution of MAA was also compared with angiographic results and with the distribution of 201Tl on images obtained in patients at rest or on redistribution images obtained before and soon after intervention in 22 patients. In control patients and those studied after aborted or unsuccessful intervention, scintigraphic results showed excellent correlation with the angiographic anatomy and were without serial change. When MAA was injected into the uninvolved vessel, the scintigram revealed evidence of collateral perfusion with retraction of the perfusion zone from that of the involved coronary in 19 of 33 patients undergoing PTCA and in three of eight of those receiving ICSK. When MAA was injected into the involved artery, a relative increase in perfusion was seen in eight of 10 patients after PTCA. Although 30 patients demonstrated scintigraphic evidence of collateral vessels, only 10 patients had angiographic evidence of collateral circulation before intervention. The distribution of 201Tl demonstrated little change in its global pattern and regions previously supplied by collaterals were generally well perfused after intervention. Coronary collateral perfusion may be inapparent angiographically and regress rapidly after angioplasty or reperfusion. Native perfusion is generally and quickly restored after successful PTCA or ICSK infusion, which obviates the need for collaterals. After intervention, the distribution of total perfusion may not change, but its regional source may demonstrate beneficial alterations, shifting from collateral to native circulation.

Intravenous and oral prenalterol in congestive heart failure. Effects on systemic and coronary hemodynamics and myocardial catecholamine balance.

Systemic and coronary hemodynamic effects of prenalterol, a beta-1 receptor agonist, were determined in patients with chronic congestive heart failure, initially after intravenous administration (10 patients) and then after oral administration (eight patients). Cardiac index increased by 33 percent and 30 percent after intravenous and oral prenalterol, respectively. The increase in stroke volume index and stroke work index and decrease in pulmonary capillary wedge pressure and systemic vascular resistance were not significant. Myocardial oxygen consumption and coronary sinus blood flow increased in the majority of patients, although these changes were not statistically significant. There were no significant changes in transmyocardial norepinephrine or epinephrine balance. The systemic and coronary hemodynamic effects of both intravenous and oral prenalterol were similar. Major side effects included sudden death (two patients) and hypotension and bradycardia (three patients) during oral prenalterol treatment. It is concluded that improved left ventricular function following both intravenous and oral prenalterol may be associated with increased myocardial oxygen consumption, and serious adverse effects may occur during prenalterol therapy.

Left ventricular volumes determined by two-dimensional echocardiography in a normal adult population.

The purpose of this study was to determine normal population volume variables of the left ventricle as determined by different algorithms currently available. Two-dimensional echocardiography was prospectively performed on 52 normal volunteers to determine normal left ventricular volume and ejection fraction as a prerequisite to their clinical application. All echocardiograms were performed using a commercially available two-dimensional phased array sector scanner. Three algorithms were applied to three views in various combinations. Ejection fraction calculations were found to be reliable, reproducible and independent of the algorithm employed. Left ventricular volumes were larger in men than in women (probability [p] less than 0.005) despite correcting for body surface area, indicating the need for separating patients according to sex. The Simpson's rule algorithm resulted in smaller values for left ventricular volume than did any of the area-length algorithms and the data were the most reproducible as judged by intraobserver variation. The single plane area-length methods are clinically useful because they are simple, rapid to execute and reliable. Ejection fraction calculation was independent of the algorithm employed.