Stephen Mallon

Clinical, electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest.

Abstract Of 352 prehospital cardiac arrest patients studied during a three year period, the initial mechanism recorded by rescue personnel was ventricular fibrillation in 220 (62 per cent), ventricular tachycardia in 24 (7 per cent) and bradyarrhythmias or asystole in 108 (31 per cent). Early survival was best in the group with ventricular tachycardia (16 of 24 patients resuscitated and survived hospitalization—67 per cent); the prognosis was worst in the group with bradyarrhythmias asystole (nine of 108 admitted to the hospital alive—none survived hospitalization); and 51 of 220 patients with ventricular fibrillation (23 per cent) were resuscitated and survived subsequent hospitalization, a significantly better outcome than previously reported for ventricular fibrillation. Central nervous system damage accounted directly or indirectly for 28 of 48 in-hospital deaths (59 per cent), and hemodynamic abnormalities for 31 per cent. Only five in-hospital deaths (10 per cent) were primary arrhythmic. The majority of survivors had evidence of left ventricular hemodynamic abnormalities (mean left ventricular end-diastolic pressure=17.80 ± 8.99 mm Hg; mean cardiac index=2.62 ± 0.72 liters/min/m 2 ; mean ejection fraction=38.58 ± 17.55 per cent), but approximately one third of the surviving patients had normal left ventricular function. Early in-hospital electrophysiologic data demonstrated persistent, drug-resistant complex ventricular arrhythmias during the first 72 hours; but intracardiac electrophysiologic studies elicited specific patterns only in patients with ventricular tachycardia, whose arrhythmias were reproducible in five of six patients studied. The risk of recurrent ventricular fibrillation in the first 72 hours was predicted better by coexistent conducting system abnormalities, than by the persistent ventricular arrhythmia alone. We conclude that the electrical mechanism of prehospital cardiac arrest provides early prognostic information, that early survival rates are improving and that one third of the discharged survivors have normal indices of left ventricular function. The presence of conducting system abnormalities identifies a subgroup at high risk for in-hospital recurrent ventricular fibrillation.

Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm.

BACKGROUND Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however. METHODS As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary-artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary-artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary-artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques. RESULTS Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary-artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested. CONCLUSIONS Silent myocardial ischemia due to coronary-artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary-artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary-artery lesions remains to be defined.

Anomalous coronary arteries: angiographic findings in 80 patients

Among 13010 adults who underwent coronary arteriography, 80 (0.61%) patients had a total of 83 anomalous coronary arteries. Thirty-three (41%) of the patients were of Hispanic origin, while out of the entire population studied 30% were Hispanic. The right coronary artery was the most common anomalous vessel. It was identified in 50 (62%) patients, arising in 35 from the left aortic sinus, in 14 from the posterior sinus, and in 1 from the left coronary artery. An anomalous circumflex artery was recognized in 22 (27%) patients. Nine (11%) patients presented an anomalous left anterior descending artery, 1 patient an anomalous left main coronary artery, and another an anomalous septal perforator artery. Twenty-three (29%) patients had concomitant congenital heart abnormalities, most commonly. bicuspid aortic valve and mitral valve prolapse. In each of 5 patients with complex congenital heart disease the course of the anomalous vessel could have interfered with a surgical procedure. In 4 cases anomalous coronary arteries were associated with either anomalous systemic venous circulation or anomalous cardiac veins. In 5 (6%) patients only, the anomalous coronary artery was solely responsible for a clinical event. Coronary atherosclerosis of the anomalous arteries was found in 28% of the patients, while the overall incidence of the disease in this series was 65%. Thus, anomalous coronary arteries are associated with a high incidence of congenital heart diseases, but do not appear to be associated with an increased risk for development of coronary atherosclerosis. The angiographic recognition of these vessels is important in patients who undergo coronary angioplasty or cardiac surgery. Variations in the frequency of congenital coronary anomalies as reported herein may be attributed to a genetic background.

Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter-fibrillation in the Wolff-Parkinson-White syndrome.

In a group of 36 consecutive patients with the Wolff- Parkinson-White (WPW) syndrome undergoing electrophysiological studies because of paroxysms of reciprocating tachycardia (RT) and/or atrial flutter-fibrillation (AF), 7 patients (19%) had repeated episodes of spontaneous alternation between RT and AF. Electrophysiological studies demonstrated left-sided anomalous pathways (AP) in all 7 patients. Atrial vulnerability, as evidenced by the occurrence of repetitive atrial responses or a paroxysm of AF following a single atrial premature stimulus, was also noted in all. Invariably, spontaneous conversion of RT to AF (7 patients) was triggered by an atrial premature depolarization which resulted in atrial asynchrony during the atrial vulnerable phase. In contrast, spontaneous conversion of AF to RT (3 of the 7 patients) required the presence or the development of antegrade unidirectional block in the AP prior to the cessation of AF. The demonstration of atrial vulnerability in association with the phenomenon of spontaneous alternation between RT and AF provides further information pertaining to the understanding of the mechanisms of tachyarrhythmias in the WPW syndrome. It is suggested that the occurrence of this electrophysiological phenomenon may be more common than is generally appreciated, and optimal medical treatment should be directed toward controlling both RT and AF in this group of Wolff-Parkinson- White patients.

The effects of intravenous verapamil on hemodynamic status of patients with coronary artery disease receiving propranolol.

Verapamil has been used clinically as an antiarrhythmic and antianginal agent. However, the intrinsic negative inotropic properties of verapamil could preclude its use in patients with coronary artery disease concurrently receiving β-adrenergic blocking agents. To investigate this possibility, 20 patients with coronary artery disease and normal left ventricular function receiving chronic propranolol therapy were given i.v. verapamil (0.025, 0.05, or 0.1 mg/kg over 2 minutes, followed by 0.005 mg/kg/min infusion) and the hemodynamic and angiographic effects were studied. The mean (± SD) plasma verapamil concentration at the time the hemodynamic effects were being measured was 122 ± 51 ng/ml for the 10 patients who received low doses (0.025 or 0.05 mg/kg) and 214 ± 108 ng/ml for the 10 patients who received high doses (0.1 mg/kg). Verapamil reduced mean arterial pressure by 22% (p < 0.001), systemic vascular resistance by 24% (p < 0.001), mean pulmonary artery pressure by 16% (p < 0.01), and pulmonary vascular resistance by 23% (p < 0.001) in all 20 patients. Concomitant increases in cardiac index, mean velocity of circumferential fiber shortening, and ejection fraction (due to the unloading effect of verapamil) were not observed. These results were not significantly different between the two dosage levels. The combined negative inotropic effects of verapamil and propranolol are of negligible importance; however, the lack of improvement in the indexes of the left ventricular function suggests some myocardial interaction of these two drugs, which may be of concern in cardiac patients with evidence of depressed myocardial performance.

Mode of initiation of reciprocating tachycardia during programmed ventricular stimulation in the Wolff-Parkinson-White syndrome: With reference to various patterns of ventriculoatrial conduction

Abstract The mode of initiation of reciprocating tachycardia in relation to various patterns of ventriculoatrial (V-A) conduction induced by programmed right ventricular stimulation was systematically analyzed in 29 patients with the Wolff-Parkinson-White (WPW) syndrome, type A. His bundle activity and atrial electrograms near the atrial ends of the normal and accessory pathways were simultaneously recorded. V-A conduction time was plotted as a function of premature ventricular coupling intervals. Four groups of patients were observed. In Group I, four patients with absence of V-A conduction, reciprocating tachycardia could not be elicited. In Group II, three patients with persistent retrograde atrial fusion from the normal and accessory pathways, reciprocating tachycardia could not be elicited because of a constant impulse collision at the atrial level. In Group III, seven patients with predominant or exclusive V-A conduction over the normal pathway, concealed retrograde penetration of the accessory pathway might have prevented the initiation of reciprocating tachycardia in all patients. In Group IV, 15 patients with predominant or exclusive V-A conduction over the accessory pathway, reciprocating tachycardia could be elicited only in 7, and its initiation appeared to depend upon the depth of retrograde penetration of the normal pathway; the less the depth of such penetration, the easier it was to elicit a reciprocating tachycardia. Furthermore, with the production of progressively less deep retrograde penetration of the normal pathway, development of repetitive ventricular responses at short ventricular coupling intervals and shortening of the ventricular driving cycle length favored the induction of reciprocating tachycardia in patients in this group. The study demonstrates that the initiation of reciprocating tachycardia during programmed ventricular stimulation in patients with the WPW syndrome is related to various patterns of V-A conduction.

Young adult survivors of sudden cardiac arrest: Analysis of invasive evaluation of 22 subjects

Twenty-two young adult (mean age 27.8 +/- 5.3 years) survivors of sudden cardiac arrest underwent invasive cardiac assessment. Initial evaluation by cardiac catheterization, coronary angiography, and hemodynamic studies identified two groups of young survivors. The first consisted of 13 (60%) subjects who had definable structural cardiac or lung disease accountable for a cardiac arrest event. Dilated cardiomyopathy dominated this group. Mitral valve prolapse, hypertrophic cardiomyopathy, left ventricular hypertrophy, anomalous origin of the right coronary artery, and tetralogy of Fallot were also encountered. The second group included nine subjects (40%) with normal cardiac structure and normal hemodynamic parameters. Electrophysiologic testing demonstrated in three of these patients the presence of Wolff-Parkinson-White syndrome. The electrophysiologic studies had a higher yield in reproduction of life-threatening arrhythmias among the subjects in the second group as opposed to the first group. The observation that 10 subjects (45%) from both groups had preceding symptoms varying from palpitations and chest pain to syncope and recurrent cardiac arrest events, is in contradiction to previous findings in the literature and raises a question of appropriate evaluation of young adults with cardiac symptoms.

Factors affecting late survival after surgical remodeling of left ventricular aneurysms

OBJECTIVES Surgical remodeling of the left ventricle has involved various techniques of volume reduction. This study evaluates factors that influence long-term survival results with 3 operative methods. METHODS From 1979 to 2000, 157 patients (134 men, mean age 61 years) underwent operations for class III or IV congestive heart failure, angina, ventricular tachyarrhythmia, and sudden death after anteroseptal myocardial infarction. The preoperative ejection fraction was 28% +/- 0.9% (mean +/- standard error), and the pulmonary artery occlusive pressure was 15 +/- 0.07 mm Hg. Cardiogenic shock was present in 26 patients (16%), and an intra-aortic balloon pump was used in 48 patients (30%). The type of procedure depended on the extent of endocardial disease and was aimed at maintaining the ellipsoid shape of the left ventricle cavity. In group I patients (n = 65), radical aneurysm resection and linear closure were performed. In group II patients (n = 70), septal dyskinesis was reinforced with a patch (septoplasty). In group III patients (n = 22), ventriculotomy closure was performed with an intracavitary oval patch. RESULTS Hospital mortality was 16% (25/157) and was similar among the groups. Actuarial survival up to 18 years was better with a preoperative ejection fraction of 26% or greater (P =.004) and a pulmonary artery occlusive pressure of 17 mm Hg or less (P =.05). Survival was worse in patients who had intra-aortic balloon pump support (P =.03). Five-year survival for all patients in group III was higher than for patients in group II (67% vs 47%, P =.04). CONCLUSIONS Factors that improved long-term survival after left ventricular surgical remodeling were intraventricular patch repair, preoperative ejection fraction of 26% or greater, and pulmonary artery occlusive pressure of 17 mm Hg or less without the need for balloon pump assist.

Comparison of Long-Term Results of Carpentier-Edwards and Hancock Bioprosthetic Valves

The long-term survival following valve replacement with Carpentier-Edwards or Hancock bioprostheses was compared between the two valve models and between the two groups totaling 407 patients who were discharged after valve replacement beginning in 1974. The two groups of patients were treated in a nonrandomized fashion. The actuarial survival for 299 patients with Carpentier-Edwards valves was 94 +/- 1.5% (+/- standard error) and 93 +/- 1.7% after 5 and 8 years of follow-up, respectively. Comparable figures for 108 patients undergoing valve replacement with Hancock valves were 89 +/- 3.0% and 83 +/- 3.7%, respectively (p = not significant [NS]). The probability of freedom from death and valve removal after 5 and 8 years of follow-up was 91 +/- 1.8% and 79 +/- 4.6%, respectively, with the Carpentier-Edwards valve and 84 +/- 3.5% and 75 +/- 4.3%, respectively, with the Hancock valve (p = NS). An accelerated rate of attrition for both valves was observed in the mitral position. There were no significant differences in actuarial survival between the two valves in the mitral or the aortic position or in the incidence of major valve-related complications.

Failure of Hancock Xenograft Valve: Importance of Valve Position (4- to 9-Year Follow-up)

To evaluate long-term durability of Hancock valves, we reviewed our results in 107 hospital survivors (120 valves) who were operated on during 1974 through mid-1979. Mitral valve replacement was done in 63 patients, aortic valve replacement in 20, and mitral valve replacement combined with other procedures in 24. The 7-year survival was 84 +/- 4% (standard error of the mean) for 91 patients and 97 valves. During a follow-up of 590 patient-years, 15 (12 mitral and 3 aortic) of 120 valves at risk (87 mitral, 32 aortic, 1 tricuspid) were removed from 14 patients. Six valves (3 mitral and 3 aortic) were removed because of bacterial endocarditis. One mitral valve was removed because of thromboembolism. Eight mitral valves were removed because of valve structural failure, which occurred at a mean follow-up of 42 months. These valves showed extensive calcification, leaflet perforation, or cusp tear. Structural failure was unrelated to valve size, year of implantation, or valve shelf-life. Structural failure was not seen after aortic valve replacement. Results show that structural failure of the Hancock xenograft valve in the mitral position is related primarily to valve position. After aortic valve replacement, valve failure is predominantly due to endocarditis. Although medium-term (mean, 6-year) durability of this xenograft valve compares satisfactorily with prosthetic valves, its high failure rate in the mitral position indicates the necessity for improvement in valve mounting, design, and preservation.