Steven G. Meister

Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris

Although intracoronary thrombus formation plays a major role in acute transmural myocardial infarction (MI), its occurrence in unstable angina (UA) and nontransmural MI has not clearly been established. To determine whether intracoronary thrombus does occur in these syndromes, coronary arteriography was performed before, during, and after intracoronary nitroglycerin and streptokinase infusion in 17 patients. None of the 8 patients with nontransmural MI and 1 of the 9 patients with UA responded to intracoronary nitroglycerin. Seven of 8 patients with nontransmural MI and 4 of 9 patients with UA responded to streptokinase infusion with opening of an occluded vessel, an increase in stenotic diameter, dissolution of an intracoronary filling defect, or a combination of these. Serial opening and closing of ischemia-related vessels occurred spontaneously and in response to streptokinase in some patients in whom thrombolysis was demonstrated. Evidence of thrombolysis was not seen in any patient studied longer than 1 week from the onset of the rest pain syndrome. The finding of thrombolysis in several patients with nontransmural MI and UA suggests that intracoronary thrombus formation plays a pathogenetic role in some patients with these ischemic syndromes.

Frequency of intracoronary filling defects by angiography in Angina pectoris at rest

Recent studies have shown that pain at rest in patients with unstable angina pectoris is often caused by transient reduction in regional myocardial perfusion. Coronary spasm has been implicated as a mechanism of this phenomenon. Recent reports have documented the occurrence of intracoronary thrombus in patients with unstable angina. Previous surveys have estimated a 6 to 12% frequency of intracoronary thrombus in this syndrome, but have not examined whether this incidence is related to how recent the angina at rest was. Angiograms of 119 patients with unstable angina who had rest pain within 14 days of angiography and 35 patients with stable angina were surveyed. Patients with unstable angina were subgrouped according to how recent angina at rest was at the time of angiography. Group I consisted of 44 patients in whom rest pain occurred within 24 hours before angiography. The 75 patients in group II had angina at rest between 1 and 14 days before angiography. Patients in group II had stable angina. The angiographic criterion for intracoronary thrombus was an intraluminal filling defect, surrounded by contrast medium on 3 sides, located just distal to or within a coronary stenosis, as assessed by each of 2 independent observers blinded to the nature of the anginal syndrome and its temporal proximity. Intracoronary thrombi were found in 44 of 119 patients with unstable angina (37%) and 0 of 35 patients with stable angina (p less than 0.00002). Intracoronary thrombi were found in 23 of 44 patients (52%) in group I and 21 of 75 (28%) in group II (p less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnostic Sensitivity of Laboratory Findings in Acute Pulmonary Embolism

Abstract Many different laboratory tests have been used to screen patients for pulmonary embolism. The sensitivity of certain laboratory tests was assessed in a prospective study of 50 patients wit...

Paradoxical embolism: Diagnosis during life☆

Abstract Of 128 reported cases of paradoxical embolism, only twelve have been diagnosed during life. However, five cases of paradoxical embolism have been detected during life at this hospital in two years. These five cases are presented to illustrate the pathophysiologic features that allow detection of paradoxical embolism during life. All five patients had unexplained arterial embolism. None had associated atrial fibrillation, mitral stenosis or myocardial infarction. Each had venous thrombosis. Two patients had congenital heart disease, whereas in three the defect permitting paradoxical embolism was a patent foramen ovale. Each patient was treated to prevent further embolism. Three did well and were discharged. Two died, and at postmortem examination, the clinical diagnosis was confirmed. The detection of five cases in two years indicates that this treatable cause of systemic embolism is substantially more frequent than indicated by the literature.

Effect of calcium-binding additives on ventricular fibrillation and repolarization changes during coronary angiography.

Ventricular fibrillation during coronary angiography with Renografin-76 (meglumine sodium diatrizoate) has been attributed to the calcium-binding additives sodium citrate and sodium ethylenediaminetetraacetic acid (EDTA), which may produce repolarization changes manifested as prolongation of the QT interval. Angiovist-370 is a newer form of meglumine sodium diatrizoate that contains calcium EDTA as its additive and thus has a decreased calcium-binding effect. Eight hundred sixteen patients were prospectively randomized to receive either Renografin-76 or Angiovist-370. Ventricular fibrillation occurred in 10 of 410 patients receiving Renografin-76 and in 0 of 406 patients given Angiovist-370 (p less than 0.0005). Clinical data were analyzed without knowledge of other data in the 10 patients treated with Renografin-76 who had ventricular fibrillation (Group I), 103 randomly selected patients who also received Renografin-76 but had no ventricular fibrillation (Group II) and 108 randomly selected patients given Angiovist-370 (Group III). Of several variables examined, only the QT interval differentiated patients receiving Renografin-76 and Angiovist-370. The mean corrected QT interval (QTc interval) before coronary angiography was slightly but not significantly (p = 0.7) higher in Group I than in Groups II and III. Ten seconds after the first left coronary artery injection it was more prolonged in Groups I and II (0.552 and 0.561 second, respectively) than in Group III (0.448 second) (p less than 0.00005). Similarly, 10 seconds after the first right coronary artery injection it was significantly longer in Groups I and II (0.545 and 0.544 second) than in Group III (0.477 second) (p less than 0.00005).(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of ventricular tachycardia by procainamide in patients with coronary artery disease

Fifteen consecutive patients with coronary artery disease had rapid (158 to 272 beats/min) and sustained ventricular tachycardia induced by the extrastimulus technique, and received procainamide infusion. Before the study, all but one patient had severe symptoms with tachycardia, and six had survived apparent sudden death. Procainamide consistently slowed ventricular tachycardia. However, in traditional doses (1 g infusion, plasma concentration greater than 4 micrograms/ml), it prevented induction of ventricular tachycardia in only 2 of the 15 patients. Induction of ventricular tachycardia was facilitated by procainamide in 10 patients. Larger doses of procainamide (plasma concentration 20.2 micrograms/ml +/- 9.7 [mean +/- standard deviation]) prevented induction of ventricular tachycardia in one of eight patients. Rapid ventricular rates (more than 210 beats/min) that were not slowed (by 50 percent or more) after a 1 g infusion of the drug predicted failure of procainamide to prevent ventricular tachycardia. Therefore, procainamide slowed but did not prevent induced ventricular tachycardia in most of these patients with coronary artery disease at risk of sudden death.

Propranolol in mitral stenosis during sinus rhythm.

Patients with early symptomatic mitral stenosis usually suffer from pulmonary congestion on the basis of left atrial and pulmonary venous hypertension. They are often in sinus rhythm, and cardiac output is usually well maintained. Symptoms occur most often when heart rate, cardiac output, or both are increased. In this study, intravenous propranolol administered to patients with pure mitral stenosis in sinus rhythm resulted in significant reductions in mitral diastolic gradient (-7.1 mm. Hg +/- 1.6 SED), mean pulmonary wedge pressure (--6.9 mm. Hg +/- 1.2) and mean pulmonary artery pressures (--9.0 mm. Hg +/- 1.2). This was due to simultaneous reduction of heart rate (--13.0 beats/minute +/- 2.6 and cardiac output (--0.5 L./minute +/- 0.2). A small associated reduction of left ventricular systolic pressure (--5.1 mm. Hg +/- 2.6) was not accompanied by adverse clinical effects. A potential role for propranolol in medical management of pure mitral stenosis in the presence of sinus rhythm is suggested.

Ventricular extrastimulation in the mitral valve prolapse syndrome. Evidence for ventricular reentry.

Fourteen patients with mitral valve prolapse and essentially normal coronary arteries were evaluated for ventricular arrhythmias, utilizing programmed ventricular extrastimulation. Three were symptomatic with ventricular tachyarrhythmias. Application of appropriately timed ventricular extrasystoles initiated the tachyarrhythmias in these three patients. The remaining eleven mitral prolapse patients were apparently free of tachycardias. Repetitive ectopic beats were not induced by extrastimulation in these eleven patients. The initiation of ventricular tachyarrhythmias by extrastimulation suggests a reentrant mechanism for the ventricular ectopy of mitral valve prolapse.

Frequency and importance of unprovoked coronary spasm in patients with angina pectoris undergoing percutaneous transluminal coronary angioplasty

Abstract Coronary spasm superimposed on fixed coronary artery stenosis was discovered in 14 of 74 candidates for percutaneous transluminal coronary angioplasty (PTCA). In 3 of the 14, spasm developed during PTCA and was presumably catheter-induced. Eleven of the 14, with unprovoked spasm, are the subject of this study. Three of the 11, in whom the fixed component of the mixed stenosis was subcritical were treated medically, with good results in 2 but with persistent angina pectoris and eventual myocardial infarct in 1. Nitroglycerin administered by the intracoronary route relieved spasm resistant to sublingual nitroglycerin in 1 of the 3. In 8 of the 11 with critical fixed stenosis, spasm was discovered either before PTCA (7 patients) or on follow-up (1 patient). Six of the 8 had successful PTCA, with no or mild symptoms on follow-up. Of the 2 failures, 1, uncomplicated, was followed by successful elective coronary artery bypass surgery while the other, complicated, led to successful emergency coronary artery bypass surgery, with disappearance of symptoms in both. The rate of success was similar in patients with documented unprovoked spasm (6 of 8) and patients without (39 of 63, 62%). It is concluded that (1) coronary spasm, if properly sought for, is probably not uncommon in single-vessel candidates for PTCA; (2) patients considered candidates for PTCA should have intracoronary nitroglycerin administered before PTCA; (3) in patients with critical, fixed coronary artery disease, associated spasm does not reduce the chances of successful PTCA; (4) coronary spasm may outlast the relief by PTCA of the fixed component of the mixed stenosis and requires long-term vasodilator therapy; and (5) the lack of adverse effects when PTCA is performed in patients with spasm superimposed on critical fixed single-vessel stenosis appears to justify its use for the time being.

Electrophysiologic effects of hydralazine on sinoatrial function in patients with sick sinus node syndrome.

The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 +/- 4.1 beats/min (mean +/- standard error of the mean) to 68.6 +/- 4.9 (P less than 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 +/- 1,098 to 2,064 +/- 573 msec (P less than 0.05) and second escape cycles shortened as well (P less than 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure (r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 +/- 692 to 1,705 +/- 382 msec (P less than 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.