Pseudoaneurysm of the ascending aorta following cardiac surgery.

Pseudoaneurysm of the ascending aorta is an unusual and potentially fatal complication of cardiovascular surgery. Most pseudoaneurysms are associated with aortic valve or coronary artery bypass graft surgery and are often mycotic in origin. Chest roentgenography and aortography have been the principle methods of diagnosis. Recently, contrast enhanced computed tomography (CT) has proven to be a useful means of diagnosis, providing a less invasive method of distinguishing pseudoaneurysm from other causes of fever and mediastinal widening in the postoperative cardiovascular patient. Thirty one cases of postoperative pseudoaneurysm of the ascending aorta occurring since 1963 are reviewed, including seven cases from our experience.

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)

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)

Late induction of tachycardia in patients with ventricular fibrillation associated with acute myocardial infarction.

A prospective study was made of 57 asymptomatic patients, 1 to 24 months after acute myocardial infarction, 17 with (Group I) and 40 without (Group II) ventricular fibrillation during the acute event. None of the 57 patients had symptomatic arrhythmias, uncontrolled heart failure or unstable angina. There was no significant difference between the two patient groups in time from acute myocardial infarction, medication used or left ventricular ejection fraction. Repetitive forms of arrhythmia (Lown grade 4) were more prevalent (29 versus 16%, not significant) during 24 hour ambulatory monitoring in patients in Group I (ventricular fibrillation group). Programmed extrastimulation was performed using 1 to 3 twice-threshold, 2 ms decremental extrastimuli delivered during right ventricular drive. Of the 17 patients in Group I, 8 had no induced arrhythmia (less than or equal to 4 extra responses), 4 had nonsustained ventricular tachycardia and 5 had sustained ventricular tachycardia (degenerating into ventricular fibrillation requiring electrical reversion in 4). None of the 40 patients in Group II had induced sustained ventricular tachycardia (p less than 0.005), although 9 had nonsustained ventricular tachycardia. Patients with ventricular fibrillation during acute myocardial infarction may have an increased risk for ventricular tachycardia or ventricular fibrillation that may be exposed by programmed electrical stimulation even when not yet clinically manifest.

Intravenous versus intracoronary streptokinase for acute transmural myocardial infarction.

In order to compare the thrombolytic efficacy of selective versus systemic administration of streptokinase, we gave this drug by either the intracoronary or intravenous routes to 25 patients during the first 6 hours of acute myocardial infarction. All patients had total occlusion of the infarct-related vessel, unresponsive to intracoronary nitroglycerin. Twelve patients received intravenous streptokinase and 13 received intracoronary administration of the drug. Angiograms were taken prior to and during streptokinase administration. Reopening was achieved in 11 of 13 intracoronary patients and 8 of 12 intravenous patients (P = Ns). Time to reopening was longer (54 minutes) in the intravenous patients than in the intracoronary patients (26 minutes) (P less than 0.05). In this study, intravenous streptokinase reopened infarct-related vessels nearly as often as intracoronary streptokinase, but it took longer. Given the limited access and time to prepare for intracoronary infusion and the ease of intravenous administration, further study of intravenous streptokinase is justified.

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.

Simultaneous contrast imaging of the left ventricle by two-dimensional echocardiography and standard ventriculography.

Simultaneous contrast two-dimensional echocardiograms and contrast ventriculograms were analyzed for 19 cardiac cycles in 6 patients. Ventriculographic volume was underestimated by 10 +/- 4.5% (p less than .001) by the contrast echocardiograms, despite good correlation (r = 0.88). Discrepancies could not be assigned to changes in volume between studies nor to a lack of precise endocardial definition. Simultaneous imaging demonstrated that the ultrasonic transducer was located 33 degrees cephalad to the cardiac apex. Although angiographic volume was severely underestimated, ejection fraction (r = 0.93) and stroke volume (r = 0.90) could be calculated from two-dimensional echocardiograms using regression equations.

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.

Effect of procainamide on induced ventricular tachycardia.

Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1-gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (less than 4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post-procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shortened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmic effect. Our data emphasize that antiarrhythmic drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.

Left ventricular end-diastolic pressure response to atrial pacing in idiopathic mitral valve prolapse.

The response of several parameters of left ventricular function to right atrial pacing was compared in 21 patients with idiopathic mitral valve prolapse and 10 normal patients. An inability to appropriately lower left ventricular end-diastolic pressure with increasing rates was demonstrated in the mitral valve prolapse group. This abnormality was not related to mitral regurgitation or factors other than ventricular performance per se.

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.