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Biomedical subjects

J Cinca

Publications and source records attributed to J Cinca.

At least 55 records · Page 3Linked to original sources
PubMed1987

Daily variability of electrically induced reciprocating tachycardia in patients with atrioventricular accessory pathways.

Sequential bedside electrophysiologic testing was performed over 22 hours at intervals of 1 to 2 hours in 13 patients with left-sided Kent bundles to assess possible daily variations in the capacity to electrically induce reciprocating tachycardia. In all patients the tachycardia involved the accessory pathway in retrograde atrial activation. Between midnight and early morning the more relevant findings with respect to the first testing performed at midday were a significant prolongation of the effective refractory period of the atrial (from 212 +/- 22 msec to 229 +/- 22 msec; p less than 0.01), atrioventricular node (from 235 +/- 22 msec to 285 +/- 15 msec; p less than 0.005), right ventricle (from 209 +/- 15 msec to 221 +/- 12 msec; p less than 0.001), and retrograde Kent bundle (from 278 +/- 34 msec to 294 +/- 24 msec; p less than 0.01) and a reduction of the inducibility of tachycardia from both the coronary sinus from 90% to 50%; p less than 0.001) and the right ventricle from 80% to 15%; p less than 0.001). Thus our results indicate that there exists a nocturnal protection against electrical induction of reciprocating tachycardia that is associated with a prolongation of the atrial, atrioventricular nodal, ventricular, and Kent bundle refractoriness.

Adolescent↗
PubMed1987

Effects of regional denervation on epicardial DC electrograms during coronary occlusion in pigs.

Sympathetic innervation of the normal and acutely ischemic myocardium and the effects of regional myocardial sympathetic denervation of the ischemic area on the evolving electrical changes during coronary occlusion were assessed in pigs anesthetized with pentobarbital sodium. The histofluorescence of the adrenergic nerve fibers (glyoxylic acid reaction), which in the normal myocardium were distributed in a diffuse network, decreased slightly after 45 min of occlusion of the left anterior descending (LAD) coronary artery and nearly disappeared after 2 h of ischemia. Topical application of phenol (carbolic acid, 88%) to the coronary arterial wall produced a transmural loss of catecholamine histofluorescence in the distal myocardium supplied by the phenol-treated arterial segment. Mapping of the epicardial direct current (DC) electrograms in sympathetically denervated and in nondenervated sections of the same ischemic area, using three rows of seven cotton-wick electrodes, was performed in eight pigs and validated in eight other nondenervated pigs. During 45 min of LAD occlusion, the denervated area, with respect to the nondenervated region, showed a greater decline in T-Q segment depression after 20 min of ischemia (P less than 0.0001), a lesser degree of S-T segment elevation throughout the study (P less than 0.0001), a delayed development of monophasic potentials (P less than 0.05), a minor degree of S-T segment alternans (P less than 0.0001), and a less marked, but still present, period of transient electrical recovery. Thus acute regional myocardial sympathectomy reduces the magnitude of the local electrical manifestations of acute myocardial ischemia in the in situ pig heart. Also in this model, sympathetic fibers appeared to lose the catecholamine histofluorescence after 2 h of acute ischemia.

Animals↗
PubMed1986

Risk of myocardium adjacent to infarcted myocardium: electrocardiographic, metabolic and scintigraphic evidence within the first week of acute myocardial infarction.

Atrial pacing was carried out within 5 days of an uncomplicated acute myocardial infarction (AMI) in 28 patients to detect the existence of a menaced area. A positive pacing response (at least 1.0 mm of ST-segment shift) was observed in 23 patients (82%, group I), whereas pacing results were negative in 5 (18%, group II). Pacing-induced electrocardiographic changes involved the leads affected by AMI in patients with transmural necrosis. A well-defined thallium-201 redistribution, mostly localized near or within the AMI site, was present in 10 patients from group I (43%), in 1 from group II (20%), and in 1 of 12 comparable patients (8%) in whom pacing was not performed. During pacing, abnormal lactate metabolism was observed in 11 of 17 patients from group I (65%) and in 0 of 5 from group II (0%). A 90% or greater coronary stenosis of at least 1 artery was found in 19 of 23 patients from group I (83%) and in 1 of 5 from group II (20%); 2- to 3-vessel disease (more than 70% diameter stenosis) was present in 14 patients from group I (61%) and 1 from group II (20%). During a 15-month follow-up (range 9 to 25), effort angina developed in 9 patients from group I (39%) and in none from group II. No deaths or reinfarctions occurred in either group. Thus, very early after a first AMI, most patients have a jeopardized periinfarction area that is usually associated with a critical coronary stenosis and that heralds effort angina in a significant proportion of them.

Adult↗
PubMed1986

Circadian variations in the electrical properties of the human heart assessed by sequential bedside electrophysiologic testing.

To assess the variability of the currently used electrophysiologic parameters and their possible circadian rhythm, sequential bedside electrophysiologic testing was performed during a 24-hour period, at intervals of 1 to 2 hours, in 12 patients who had normal atrioventricular (AV) conduction times and normal sinus node function. The coefficients of variation during the 24-hour period were: +/- 10.4% for the R-R interval, +/- 10.6% for the sinus node recovery time (SRT) at atrial pacing of 100 bpm, +/- 32.5% for the corrected SRT, +/- 15.1% for the ventriculoatrial (VA) effective refractory period (ERP), +/- 8.3% for the AV nodal ERP, +/- 5.7% for the AH interval, +/- 5.2% for the HV interval, +/- 5.5% for the atrial ERP, +/- 3.3% for the right ventricular ERP, +/- 2.8% for the QT interval, +/- 4% for the VA interval, and +/- 3.4% for the retrograde Kent bundle ERP. Between 12:00 midnight and 7:00 AM, there was significant lengthening of: the sinus node rate (p less than 0.0005), the SRT at atrial paced rates of 100 and 120 bpm (p less than 0.025), the QT interval duration (p less than 0.025), and the ERP of the atria (p less than 0.025), AV node (p less than 0.01), and right ventricle (p less than 0.05). Thus conventional electrophysiologic parameters are subject to daily variability and, like sinus node function, AV nodal and myocardial refractoriness follow a circadian rhythm with an acrophase between 12:00 midnight and 7:00 AM. In addition, prolonged bedside recording of the His bundle potential can be reliably obtained.

Adolescent↗
PubMed1986

Progressive mechanical impairment associated with progressive but reversible electrocardiographic ischaemic changes during repeated brief coronary artery occlusion in pigs.

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 electrically 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, 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.

Animals↗
PubMed1986

Resting angina with fixed coronary artery stenosis: nocturnal decline in ischemic threshold.

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.

Angina Pectoris↗
PubMed1985

Electrophysiologic effects of unilateral right and left stellate ganglion block on the human heart.

To determine the electrophysiologic effects of stellate ganglion (SG) block on the human heart, the two SGs were anesthetized separately, with a 24-hour interval between the two procedures, in 13 patients with episodes of supraventricular tachycardia (six had Kent bundles). Left SG block caused: (1) a lengthening of the AH interval, measured at fixed atrial rates of 10 +/- 12 msec (p less than 0.01); (2) a marked depression of the VA conduction in six of the seven patients with measurable VA interval (in two patients it produced complete VA block); (3) a slowing of 20 to 40 msec of the cycle of an electrically induced reciprocating tachycardia; and (4) failure to modify the QT interval duration. In contrast, right SG block produced asymmetric or opposite changes and prolonged the QT interval (7.6 +/- 8.8 msec, p less than 0.05). Atrial and ventricular refractoriness was not significantly altered by SG block. Retrograde effective refractory period of the Kent bundle changed 20 to 60 msec after unilateral SG blockade. Thus, this study suggests that the human conduction system and the Kent bundles receive an appreciable sympathetic influence from the SG. Like experimental studies, we also found an asymmetric response to unilateral SG block and a dominance, in most of our patients, of the left SG. The influence on myocardial refractoriness was less apparent.

Adult↗
PubMed1985

Pharmacokinetics of intravenous propafenone in patients with episodes of paroxysmal supraventricular tachycardia.

The plasma concentration time curves of propafenone after administration of single i.v. (2.3 +/- 0.2 mg/kg) doses have been studied in ten patients undergoing an electrophysiological study to evaluate episodes of recurrent supraventricular tachycardia. The propafenone kinetics profile can be described by a two-compartment open model. Mean values of main variables were t 1/2 alpha = 2.8 min, t 1/2 beta = 80 min, Kel = 0.12 min, -1, Vd beta = 1.6 1/kg, Cl = 1.03 1/h and AUR = 3.1 mg/h-1.

Adult↗
PubMed1984

Peri-infarction zone at risk during the first 5 days after an acute transmural myocardial infarction: electrocardiographic evidence.

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)

Adult↗
PubMed1984

Shortening of ventriculoatrial conduction in patients with left-sided Kent bundles.

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.

Adult↗
PubMed1984

Transmural DC electrograms after coronary artery occlusion and latex embolization in pigs.

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.

Animals↗
PubMed1983

Prolonged angina pectoris and persistent negative T waves in the precordial leads: response to atrial pacing and to methoxamine-induced hypertension.

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.

Adult↗
PubMed1983

Prognostic implications of early spontaneous angina after acute transmural myocardial infarction.

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.

Angina Pectoris↗
PubMed1981

Right ventricular infarction: relationships between ST segment elevation in V4R and hemodynamic, scintigraphic, and echocardiographic findings in patients with acute inferior myocardial infarction.

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.

Acute Disease↗
PubMed1981

Acute arterial hypertension during spontaneous angina in patients with fixed coronary stenosis and exertional angina: an associated rather than a triggering phenomenon.

The role of systemic arterial hypertension as a possible trigger of myocardial ischemia during angina at rest was studied in 13 consecutive patients who also had a history of exertional angina. Significant (greater than or equal to 70%) stenosis of at least one major vessel was present in each of the 10 patients in whom coronary arteriography was carried out. After documentation of the electrocardiographic and arterial blood pressure changes during two or more episodes of resting angina, i.v. methoxamine was infused under continuous monitoring of the ECG, arterial blood pressure and pulmonary artery diastolic pressure. The heart rate was maintained either spontaneously or by atrial pacing to levels similar to those during angina at rest. Despite increases in arterial blood pressure and the double product (systolic blood pressure x heart rate) to levels higher than those during spontaneous angina in all patients, no chest pain or electrocardiographic changes occurred in nine patients. In the other four patients, however, angina supervened. Three of these four patients, but only one of the remaining nine, had a borderline or elevated pulmonary artery diastolic pressure at rest. We conclude that in a considerable number of patients with "nonvariant" resting angina, acute increases in arterial blood pressure during the spontaneous attacks are not likely to be the cause of myocardial ischemia. Nevertheless, in some of these patients, increases in resting pulmonary artery diastolic pressure may favor the development of ischemia during afterload augmentation.

Acute Disease↗
PubMed1980

Reciprocating tachycardia using bilateral anomalous pathways: electrophysiologic and clinical implications.

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.

Adult↗