Search

Clinical and electrophysiologic features of acute ischemic right bundle-branch block (RBBB) that are reversible by His bundle pacing were analyzed in nine patients. All had large anterior myocardial infarctions (mean peak CK-MB = 185 +/- 71 IU/l), and six showed increased pulmonary capillary pressures. The RBBB occurred within 48 hours of infarction, and in six patients it was associated with left fascicular block. The HV intervals that were measured 1 to 4 days after infarction were normal in all patients. Progression to complete atrioventricular (AV) block occurred in three patients, and one patient required permanent cardiac pacing. Sustained ventricular tachycardia developed in two patients, and ventricular fibrillation developed in five. During a mean follow-up period of 26 months, four patients died (three of them suddenly). The RBBB disappeared in only one case. Acute ischemic intraHisian RBBB occurred in the setting of massive myocardial infarctions complicated by ventricular tachycardia or fibrillation and by a high mortality rate during the follow-up period. The RBBB rarely reverted spontaneously, and the His-Purkinje conduction time was frequently normal.

Cardiac refractoriness and electrical inducibility of supraventricular tachycardia (SVT) were assessed at intervals of 1 to 2 hours over a period of 22 hours in 38 patients (25 with paroxysmal SVT). Daily variability of effective refractory period (ERP) had a mean range of 35 +/- 14 mseconds for the atria, 79 +/- 65 mseconds for the AV node, 24 +/- 10 m seconds for the ventricles, 51 +/- 27 mseconds for the retrograde Kent bundle, and 35 +/- 17 mseconds for the antegrade Kent bundle. Between 11 PM and 8 AM there was a significant prolongation of the ERP of the atria (ANOVA, p less than 0.001), AV node (p = 0.002), right ventricle (p less than 0.001), and retrograde Kent bundle (p = 0.005), and a reduction in electrical induction of SVT from 75% to 42% (p less than 0.05) with respect to the first electrophysiologic study. This nocturnal prolongation was preceded by ERP shortening of all explored cardiac sites and by increased tachycardia inducibility between 8 and 10 PM. Six patients with dual AV nodal pathways showed a prolongation of the fast pathway ERP at midnight, whereas conduction through the slow pathway followed an unpredictable daily variability. These data indicate a circadian influence on refractoriness of normal cardiac tissues and accessory pathways that exerted a midnight protection against electrical inducibility of reciprocating tachycardia but a transient arrhythmia facilitation at the evening.

The relationship between ST segment elevation on the right precordial lead V4R and the hemodynamic, echocardiographic, and myocardial scintigrapic signs suggestive of right ventricular (RV) infarction was studied in 42 patients with acute inferior myocardial infarction. Twenty-two patients had ST segment elevation in V4R. Among these patients, a significant correlation was demonstrated between V4R ST segment elevation and the hemodynamic (p less than 0.001), scintigraphic (p less than 0.001), and echographic (p less than 0.02) criteria for acute RV infarction. These results support the validity of this new electrocardiographic sign as a practical means in aiding the clinical detection of RV involvement with acute transmural inferior myocardial infarction.

Atrial pacing was performed in 16 patients with angina at rest and significant coronary artery stenosis (greater than 70%) over 2 consecutive days in the morning (10 A.M. to 1 P.M.), in the afternoon (4 to 7 P.M.), and at night (12 midnight to 3 A.M.) to assess possible circadian variations of their ischemic threshold. Overall, the incidence of resting angina was highest at night. All pacing results were positive (greater than or equal to 1.0 mm ST segment shift) and tended to be reproducible in nine patients, whereas some or all were negative in seven. Among all positive results, ischemic thresholds at night were significantly lower than those in the morning and in the afternoon (125 +/- 3 vs 138 +/- 3 and 139 +/- 2 beats/min, mean +/- SEM; p less than .005). In nine patients, 19 pacing tests produced ST segment elevation, of which 13 were performed at night (68%). We conclude that patients with resting angina and severe coronary stenosis often exhibit a nocturnal decline in their ischemic threshold, which seems to facilitate development of transmural ischemia during atrial pacing.

Acute elevation of the ST segment in several ECG leads was observed in seven patients with bacterial shock during the course of therapy. Six patients had bacterial pneumonia, one had acute cholecystitis, and none had a previous history of heart disease. At the onset of the ST elevation, all patients were receiving dopamine infusion, which in four of them was inadvertently increased shortly before the ECG changes, the ST elevation was not associated with chest pain, pericardial friction rub, or acute changes in the heart rate, or arterial blood pressure. In four patients the maximum ST elevation was greater than or equal to 5 mm. In each instance the ST segment returned to the isoelectric line within 24 hours, and subsequent development of Q waves or changes in the QRS was not observed. Although the existence of an acute pericarditis or an acute myocarditis as possible causes of the ST elevation cannot be fully ruled out, the sudden onset, prominent magnitude, and brief duration of the ST elevation are perhaps more indicative of an acute ischemic event, possibly related to a transient coronary vasoconstriction induced by the dopamine infusion.

The sequential changes and the rate dependence of the Q-T interval were studied in 21 patients 6 hours to 5 days after an anterior (11 cases) or an inferior (10 cases) acute transmural myocardial infarction. The Q-T interval was analyzed at fixed atrial-paced heart rates in leads aVF and V3 recorded at 100 mm/s and at twice the standard amplitude. Values were compared with those of a group of normal subjects matched by age and sex. Severe ventricular arrhythmias, electrolyte or conduction disturbances and pericarditis were excluded in all patients. Sequential changes in the Q-T interval were apparent only in the leads showing the ischemic changes (lead V3 in anterior and lead aVF in inferior myocardial infarction) in 19 of 21 patients. After an initial shortening (first 12 hours), there was a remarkable lengthening of the Q-T interval coinciding with T wave inversion (12 to 24 hours after the myocardial infarction). By the 4th to the 6th day, there was a return to normal values. The lengthening of the Q-T interval was greater in anterior than in inferior myocardial infarction. The rate-dependent shortening of the Q-T interval at increasing rates was more prominent at the beginning of T wave inversion. It is concluded that lengthening of the Q-T interval is common 12 to 24 hours after the onset of an acute myocardial infarction and that prolongation of up to 20 percent over the initial values may occur in cases not complicated by severe ventricular arrhythmias.

Changes in epicardial and endocardial direct current (DC) electrograms and ventricular arrhythmias observed during 60 min of left anterior descending coronary artery (LAD) occlusion in nine anesthetized pigs were compared with those observed in eight other pigs after embolization of the LAD with latex, a procedure able to block collateral blood flow to the ischemic area. After LAD occlusion 1) T-Q segment depression and S-T segment elevation showed a faster rate of development, and monophasic potentials occurred earlier in the endocardium than in the epicardium; 2) T-Q segment depression was greater at the center than at the periphery of the ischemic area during the first 20-30 min, and later it become greater at the periphery than at the center; and 3) a period of transient recovery in the local activation beginning after 8-15 min and lasting for 10-20 min occurred in all cases, commonly associated with T-wave alternans. LAD embolization with latex induced greater T-Q and S-T segment changes in the epicardium than in the endocardium, increased the incidence of ventricular fibrillation, and failed to impede the appearance of the period of transient electrical recovery. Thus, within an acutely ischemic area in the in situ pig heart, there are inhomogeneities in the magnitude and time course of the electrical changes, which are not prevented by procedures able to block collateral blood flow to the ischemic area. Ventricular fibrillation was also not prevented by such a procedure.

An atrial pacing test was performed daily during the initial 5 days after a first myocardial infarction (MI) in 33 patients in Killip class I or II, to assess the presence of areas at risk of ischemia. Pacing caused a transient ST-segment shift of 1 mm or more in 26 patients (79%) (positive test, Group I) in the first 3.6 +/- 1.1 days after infarction, whereas no ST-segment change developed during pacing in 7 patients (negative test, Group II). Pacing-induced electrocardiographic changes were always localized in the leads involved by the MI. Right and left ventricular filling pressures were higher in Group I than in Group II (8 +/- 4 vs 5 +/- 3 mm Hg, p less than 0.05, and 16 +/- 7 vs 12 +/- 7 mm Hg, p less than 0.02, respectively). Both groups had similar increases in peak enzyme values and a similar mortality rate (2 of 26 vs 1 of 7 at an average follow-up of 16 months). The reinfarction rate was higher in Group II (3 of 7 vs 1 of 26). In 7 patients similar to the 33 patients studied, metabolic studies revealed lactate abnormalities during pacing in 4 of the 6 patients with positive test results and unchanged metabolism in the patient with a negative test result. Thus a jeopardized peri-infarction area appears to exist in most patients soon after an uncomplicated MI. Its presence is often associated with silent heart failure, but it is probably unrelated to peak enzyme increase or to prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

In 18 consecutive patients without a history of myocardial infarction (MI), prolonged angina pectoris with persistent negative T waves in the precordial leads was associated with a high frequency of in-hospital spontaneous angina (14 of 18, 78%), usually accompanied by S-T segment elevation, and occasionally in-hospital MI (4 of 18, 22%). Angina and MI always involved the electrocardiographic leads with negative T waves. Coronary arteriography, performed in 16 patients, revealed greater than or equal to 90% proximal diameter reduction of the left anterior descending (LAD) coronary artery in 14 patients. No patient had severe narrowing of all 3 major coronary arteries, but the 3 who had 100% LAD occlusion lacked collateral circulation. The ejection fraction was greater than or equal to 50% in 13 patients. Atrial pacing performed in 11 patients at an average rate of 142 beats/min produced a 1.0 mm S-T segment change in only 5 patients (45%), 3 of whom had an associated lactate production. Arterial systemic hypertension induced by methoxamine in 14 patients caused reversal of negative T waves without significant S-T segment shifts or chest pain and failed to elicit lactate extraction abnormalities in each of the 5 patients in whom it was determined. Thus, prolonged angina with persistent negative T waves in the precordial leads is almost invariably associated with a critical and proximal LAD obstruction, severe narrowing of 1 or 2 coronary arteries, and poor or absent collateral vessels. The relatively preserved coronary reserve in 55% of our patients suggests that negative T waves do not represent active myocardial ischemia. The study also suggests that transient "positivization" of the negative T waves may not necessarily relate to myocardial ischemia when associated with acute systemic hypertension.

Epicardial and endocardial electrograms, myocardial metabolism, left ventricular pressure, and regional myocardial tension were studied during 15 min coronary occlusions followed by 45 min reperfusion in the in situ pig heart to evaluate their reproducibility and the possibility of a cumulative effect. Two coronary occlusions were performed in 27 animals, three in 21, and four in nine. Throughout the different occlusions there was a progressive increase in peak TQ-ST segment shift, a progressively higher incidence of ST segment alternans, and an increasing prolongation of the ventricular activation time. Regional myocardial tension in the ischaemic area, measured in eight pigs, declined progressively after each occlusion-reperfusion cycle, whereas it failed to change in four sham experiments. Nevertheless, complete electrical recovery ensued after each reperfusion and was progressively quicker throughout the four reperfusions. In addition, lactate production due to ischaemia returned to extraction after each reperfusion when studied in eight pigs undergoing three occlusion-reperfusion cycles. It is concluded that multiple coronary occlusions in pigs causes (a) a progressive deterioration in contractility and (b) a progressive but reversible deterioration in the electrical changes. These findings may explain the impaired segmental wall motion seen in some patients with recurrent angina at rest and no evidence of infarction. In this model, however, the electrical and metabolic recovery after each reperfusion probably indicates that the gross ischaemic alterations were reversed but that a minor though probably increasing degree of tissue necrosis may have been present.

Whole serum complement (CH50) and C3, C4, and C3PA plasma values were studied in 48 patients: 9 with nonseptic shock; 20 with sepsis; 14 with septic shock caused by gram-negative bacteria; 5 with septic shock caused by gram-positive bacteria. All were compared with a control group of 25 healthy individuals. Determinations were made upon admission and again 48 and 96 h later. No significant differences in complement values were found between the patients with nonseptic shock and the control group. In the patients with sepsis, decreased CH50 (p less than 0.001) and increased C3PA (p less than 0.02) values were observed, while C3 and C4 remained unaltered. In the patients with septic shock, markedly decreased levels of CH50, C3, and C4 were seen (p less than 0.001, and p less than 0.001, and p less than 0.001, respectively) without changes in C3PA levels. There were no differences between septic shock due to gram-negative and gram-positive bacteria, or between patients who died and those who survived. After 96 h, the altered values returned to the normal range. This underlines the transitory activation of the complement system through the classic pathway and suggests its possible role in the pathogenesis of septic shock in man.

We investigated the clinical, electrocardiographic and hemodynamic features and the prognostic implications of early spontaneous angina in 31 consecutive patients after acute myocardial infarction. Re-elevation of ST segments in the area of infarction occurred during angina and during reinfarction in all but one patient. Depression of ST segments, when present during pain, involved the same leads as in the acute infarction. Blood pressure and double product tended to increase during pain in 23 patients. The magnitude of this change, however, often varied from crisis to crisis and there were no increases in these parameters in one or more attacks in 15 patients. Sublingual nitroglycerin, 1.0 mg, failed to relieve one or all anginal episodes in 17 of the 28 patients in whom it was given. In-hospital mortality rate was 10% (3/31) and always followed reinfarction. In-hospital reinfarction rate was 16% (5/31) and followed a larger number of anginal crises (7.2 +/- 1.3 vs 3.0 +/- 2.1, P less than 0.001) and a higher incidence of transient hypotensive episodes than in the rest of patients (3/5 vs 3/26). Three additional patients died after discharge. Of the remaining 25 patients and during a follow-up of 26 months (16-34) only one developed reinfarction. Early resting angina after a transmural infarction is almost invariably associated with ECG evidence of ischemia in the leads overlying the infarcted zone. The inconsistent changes in blood pressure and heart rate during pain render these hemodynamic changes an unlikely cause of this form of angina. While postinfarction angina did not carry a grave short- or long-term prognosis, patients with recurrent crises demonstrated as high a risk of reinfarction and death as those with spontaneous hypotension.

A patient who had disabling supraventricular tachycardia showed electrophysiologic evidence of coexistent right and left Kent bundles. The supraventricular tachycardia was accelerated by sequential antegrade and retrograde conduction over the right and left Kent bundles, respectively. Spontaneous blocking of the conduction through the right Kent bundle was associated with a slowing of the tachycardia and with the appearance of right bundle branch block (RBBB). Antegrade conduction was through the left bundle branch and was followed by an early retrograde atrial activation through the left Kent bundle, with consequent shortening of the ventriculoatrial (VA) interval. Thus, the coexistence of bilateral Kent bundles can be suspected whenever shortening of the VA interval in external electrocardiographic recordings occurs in the presence of a tachycardia with a RBBB pattern in a patient with right-sided preexcitation. Our data also showed that bilateral accessory pathways may have different electrophysiologic properties and that unequal response to antiarrhythmic drugs may be expected.

In six patients with electrophysiologic evidence of ventriculoatrial conduction through a left Kent bundle, we documented that programmed right ventricular stimuli falling within an interval of 60 to 160 msec from the end of the T wave propagated to the left atrium (distal coronary sinus unipolar lead) 10 to 20 msec earlier than the basic paced beats. This phenomenon could be reproduced 24 hours later in two patients, and it was abolished by procainamide and amiodarone in one instance. During this interval we were unable to induce reciprocating tachycardia. Our observations outline a new pattern in ventriculoatrial conduction in patients with left-sided Kent bundles. The findings suggest in addition, that (1) supernormal conduction may be responsible for the observed shortening in retrograde conduction and (2) this phenomenon does not facilitate induction of reciprocating tachycardia.

A case of post-traumatic coronary occlusion is presented. A 38-year-old male sustained a blunt chest trauma with secondary transmural infarct and early evolution toward a huge left ventricular aneurysm. Coronary arteriography showed complete occlusion to the left anterior descending coronary artery.