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J Cinca

Publications and source records attributed to J Cinca.

At least 37 records · Page 2Linked to original sources
PubMed1997

Local repolarization abnormalities induced by transcatheter radiofrequency ablation in pigs.

Radiofrequency (RF) ablation alters action potential repolarization of myocardial cells and, theoretically, this should induce ST-T segment changes in the ECG. Since these ECG abnormalities have been rarely reported in patients submitted to RF ablation we assess the ability of the procedure to cause ST-T segment changes in local electrograms. Epicardial ECG mapping was performed in 17 anesthetized open chest pigs submitted to endocardial (n = 9) or to epicardial (n = 8) unipolar radiofrequency ablation (500 kHz, 20 W for 5-10 s). To characterize the cellular electrophysiological alterations induced by RF ablation transmembrane action potentials were recorded at various distances from the ablation lesion; these were compared with seven control pigs. Endocardial RF ablation induced a transient (< 5 min) change of 6.1 +/- 2.4 mV in T wave amplitude (baseline: 12.8 +/- 5.6 mV, P < 0.001) in 141 out of 269 epicardial electrodes. T wave changes were associated with shortening in local activation time (20.1 +/- 2.3 ms at baseline vs 18.5 +/- 2.5 ms at 60 s after ablation, P = 0.03). RF current caused persistent St segment elevation at the center of the ablation lesion with no transmural expansion. Intracellular potentials along a 2-6 mm wide myocardial band bordering the RF lesion lower amplitude (101 +/- 7.0 mV vs 71 +/- 23 mV, P < 0.01) and shorter duration (254 +/- 44 ms vs 156 +/- 29 ms, P < 0.01) than control hearts. The center of the ablation lesion was electrically unexcitable. We concluded that RF ablation alters cellular electrophysiology in small areas surrounding the ablation lesion and this causes short-lasting transmural changes in T 3 wave amplitude and nontransmural ST segment elevation.

Action Potentials↗
PubMed1996

Neurally mediated negative inotropic effect impairs myocardial function during cholinergic coronary vasoconstriction in pigs.

BACKGROUND: Myocardial dysfunction elicited during cholinergic coronary vasospasm is generally ascribed to myocardial ischemia. However, when pericoronary nerves extend to the ventricles, efferent vagal discharges that elicit coronary vasoconstriction may, at the same time, depress myocardial contractility by releasing acetylcholine into the myocardium. We analyzed whether a neurally mediated effect contributes to impairment of ventricular function during cholinergic coronary vasoconstriction. METHODS AND RESULTS: Left ventricular (LV) function, ECG mapping, and coronary angiography were analyzed during pericoronary application of methacholine (MCh) to the left anteriors. descending coronary artery in 53 chloralose-anesthetized openchest pigs. MCh induced local coronary vasoconstriction and depressed coronary blood flow (13.3 +/- 3.7 to 6.0 +/- 4.6 mL/min [54%]; ANOVA, P < .001), systolic LV pressure (105 +/- 10 to 91 +/- 10 mm Hg [13%], P < .001), peak LV (+)dP/dt (2890 +/- 524 to 2270 +/- 447 mm Hg/s [21%], P < .001), peak LV (-)dP/dt (1446 +/- 484 to 1048 +/- 276 mm Hg/s [27%], P < .001), and regional systolic segment shortening (0.32 +/- 0.09% to 0.18 +/- 0.14% [43%], P = .02) and caused local ST-segment elevation (0.9 +/- 0.8 to 8.4 +/- 3.9 mV, P < .001). These changes were not preceded by heart rate variations, were reproducible, and were inhibited by atropine. MCh during perfusion of nitroglycerin (2 micrograms.kg-1.min-1 IV) continued to depress LV pressure (9%, P = .002), LV (+)dP/dt (16%, P < .01), LV (-)dP/dt (20%, P < .01), and segment shortening (18%, P = .03) even though coronary blood flow drop was markedly attenuated (7% versus 54%; ANOVA, P < .01). Disruption of pericoronary nerves with phenol attenuated MCh-induced LV pressure fall (P < .05). Histological data show that cholinergic and adrenergic pericoronary nerves extend into the ventricular myocardium. CONCLUSIONS: A neurally mediated effect, in addition to ischemia, impairs LV function during cholinergic coronary constriction in a model with pericoronary nerves extending into the ventricles.

Animals↗
PubMed1996

Coronary denervation attenuates coronary constriction induced by muscarinic receptor stimulation in pigs.

OBJECTIVES: We tested the hypothesis that coronary denervation attenuates the reactivity of the coronary vessel to cholinergic stimulation. METHODS: Heart rate, left ventricular (LV) pressure, LV dP/dt, coronary blood flow at the left anterior descending (LAD) coronary artery, and epicardial ECG mapping were measured before and after topical application of 1% methacholine to the LAD in 10 pigs anesthetized with alpha-chloralose (100 mg/kg, i.v.); these were compared with 10 other pigs submitted 2 weeks previously to a denervation of the LAD with phenol. Coronary denervation was confirmed in all cases by adrenergic histofluorescence and by acetyl-cholinesterase staining. Isolated LAD rings from 10 additional pigs (5 controls and 5 treated with phenol) were stimulated with endothelin-1 to verify whether phenol affected coronary reactivity to noncholinergic stimulation. RESULTS: Methacholine induced a fall in coronary blood flow (10.3 +/- 5.3 ml/min vs 4.8 +/- 6.2 ml/min, ANOVA: P < 0.001), a drop in systolic LV pressure (113 +/- 19 mmHg vs 93 +/- 19 mmHg, P < 0.001) and LV dP/dt (1608 +/- 363 mmHg/s vs 1203 +/- 302 mmHg/s, P = 0.02) and elevation of the ST segment (1.4 +/- 0.9 vs 11.1 +/- 4.7 mV, P < 0.001) in controls. These changes were not preceded by heart rate variations and were inhibited by atropine. As compared to controls, phenol-treated pigs showed a smaller decline in coronary blood flow (13.1 +/- 4.5 ml/min to 10.4 +/- 5.4 ml/min, P < 0.001), a lower drop in LV pressure (107 +/- 20 mmHg to 100 +/- 19.7 mmHg, P < 0.001) and lesser ST segment elevation (2.2 +/- 1.7 mV to 5.6 +/- 4.2 mV, P < 0.001). Isolated LAD rings contracted after exposure to endothelin-1 in both controls and phenol-treated pigs (3.5 +/- 0.7 g vs 2.4 +/- 1.0 g, P = 0.06). CONCLUSIONS: Coronary denervation attenuates coronary constriction induced selectively by direct muscarinic receptor stimulation in the in situ pig heart.

Animals↗
PubMed1996

Predisposing factors and prognostic value of sustained monomorphic ventricular tachycardia in the early phase of acute myocardial infarction.

OBJECTIVES: The purpose of the study was to analyze the factors that favor the occurrence of sustained monomorphic ventricular tachycardia in the early phase (< 48 h) of acute myocardial infarction and to establish its prognostic implications. BACKGROUND: Sustained monomorphic ventricular tachycardia early in the course of an acute myocardial infarction is an uncommon arrhythmia, and its significance has not been specifically studied. METHODS: The clinical characteristics and prognosis of sustained monomorphic ventricular tachycardia were studied in 21 (1.9%) of 1,120 consecutive patients admitted to the coronary care unit with a diagnosis of myocardial infarction. RESULTS: Patients with sustained monomorphic ventricular tachycardia had a larger infarct on the basis of peak creatine kinase, MB fraction (CK-MB) isoenzyme activity (435 +/- 253 IU/liter vs. 168 +/- 145 IU/liter, p < 0.001) and higher mortality rate (43% vs. 11%, p < 0.001). By logistic regression analysis, independent predictors of sustained monomorphic ventricular tachycardia were CK-MB (odds ratio [OR] 11.8), Killip class (OR 4.0) and bifascicular bundle branch block (OR 3.1). Moreover, sustained monomorphic ventricular tachycardia was itself an independent predictor of mortality (OR 5.0). Compared with patients with ventricular fibrillation, those with sustained monomorphic ventricular tachycardia had a worse Killip class (Killip class > I: 63% vs. 30%, p < 0.05), higher CK-MB activity (430 +/- 260 IU/liter vs. 242 +/- 176 IU/liter, p < 0.01) and higher arrhythmia recurrence rate (31% vs. 4%, p < 0.01). During the follow-up period, 5 (42%) of 12 survivors in the sustained monomorphic ventricular tachycardia group died of cardiac-related causes. Recurrence of ventricular tachycardia was seen in two patients (17%). CONCLUSIONS: Sustained monomorphic ventricular tachycardia during the first 48 h of myocardial infarction is a sign of extensive myocardial damage and an independent predictor of in-hospital mortality.

Adult↗
PubMed1995

ST segment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for passive transmission from the ischemic peri-infarction zone.

BACKGROUND: Ischemia of the myocardium surviving an infarction induces ST segment elevation in infarct-related ECG leads. In cases with no viable tissues, ischemia adjacent to the infarction could induce a similar ECG pattern if there is ST segment potential transmission through the necrotic scar. We analyzed whether acute ischemia adjacent to a healed infarction with no viable tissue may induce ST segment elevation on the surface of the necrotic scar. METHODS AND RESULTS: Epicardial ST segment changes elicited during 30 minutes of acute reocclusion of the left anterior descending (LAD) coronary artery 2 cm above the first diagonal branch were analyzed by 32-channel mapping in 18 chloralose-anesthetized open-chest pigs with 1-month-old anterior infarctions induced by permanent ligature below the first diagonal branch (group 1). The effect of a previous infarction on the magnitude of ischemic ST segment changes was assessed by similar mapping in 21 control pigs submitted to a LAD ligature 2 cm above the first diagonal branch (group 2, n = 11) or just below this branch (group 3, n = 10). Myocardial perfusion after coronary ligature was estimated in 7 pigs with chronic infarction and in 3 control pigs by mapping of myocardial technetium-99m-methoxyisobutyl isonitrile (99mTc-MIBI) activity in transmural samples underlying each epicardial electrode. The width of cell layers surviving the infarction was measured and their viability after 60 minutes of coronary reocclusion was assessed by intracellular glycogen staining. Reocclusion of the LAD induced parallel ST segment elevation at the periinfarction zone and at the necrotic scar, although in the latter region the changes were less marked (maximal ST segment, 8.4 +/- 3.0 mV versus 2.7 +/- 1.8 mV, ANOVA, P < .001). ST segment elevation inside the scar was greater at the margins (3.9 +/- 1.8 mV) than at sites 20 mm toward the center (2.8 +/- 1.7 mV, P = .003). The necrotic area was virtually devoid of surviving cells except for a 0.22 +/- 0.04-mm-wide subendocardial band that continued to show a positive intracellular glycogen reaction after the second LAD ligature. Acute ischemia adjacent to the infarction (group 1) induced lower ST segment elevation than acute ischemia at a comparable cardiac region in noninfarcted pigs (group 2) (ANOVA, P = .02), despite the fact that these areas developed similar underperfusion after coronary occlusion (percent MIBI activity of that in normal myocardium, 7 +/- 8 versus 7 +/- 6, P = NS). ST segment changes in group 2 pigs were comparable to those induced in group 3 pigs with a 2-cm-lower coronary occlusion. CONCLUSIONS: Acute ischemia adjacent to a chronic infarction induces ST segment elevation at the surface of the scar despite the virtual absence of viable tissue within the infarction. Data suggest a passive ST segment potential transmission through the infarction. Moreover, ischemia adjacent to a chronic infarction induces lower ST segment elevation than ischemia not adjacent to a necrosis. The mechanisms accounting for these regional differences are probably independent of collateral myocardial perfusion and ischemia extension.

Animals↗
PubMed1994

Low incidence of ventricular arrhythmias induced by ischaemia at the borders of a chronic infarct in a model with local postinfarction denervation.

OBJECTIVE: The aim was to assess the arrhythmogenic potential of acute ischaemia superimposed at the borders of a chronic myocardial infarct and to analyse the effects of myocardial necrosis on local autonomic innervation in pigs. METHODS: Ventricular arrhythmias were measured in alpha chloralose (100 mg.kg-1) anaesthetised open chest pigs during 60 min occlusion of the left anterior descending coronary artery 2 cm above the first diagonal branch (group I, n = 11) or just below this branch (group II, n = 12). These arrhythmias were compared with those induced in pigs with a one month old anteroseptal infarction (coronary ligature as in group II) submitted to a second occlusion 2 cm above the first (group III, n = 12). The area at risk after high or low ligature was measured in 12 control pigs using fluorescein. Sympathetic and parasympathetic innervation of the anteroseptal myocardium was studied in three pigs with a chronic anteroseptal infarction and in six pigs without infarction using adrenergic histofluorescence and acetylcholinesterase reaction. RESULTS: Compared with ischaemia alone, ischaemia at the borders of a chronic infarct induced a lower incidence of ventricular fibrillation (1/12 pigs v 11/11 in group I, p < 0.001, or 6/12 in group II, p < 0.05) and a tendency towards a lower occurrence of ventricular tachycardia (2/12 pigs v 8/11 in group I, p = 0.01, and 4/12 in group II) and fewer ventricular premature beats (mean number: 105 in group I v 30 in group III, p < 0.05). The mass of the ischaemic regions after low or high occlusion was 13.3(SD 3.0) g and 23.2(5.8) g, respectively. Adrenergic and cholinergic denervation was observed inside the necrotic area, along the subendocardium surviving the necrosis, and in a band of normal bordering myocardium [width: 3.2(2.0) mm for adrenergic and 2.1(1.2) mm for cholinergic denervation]. CONCLUSIONS: Acute ischaemia at the borders of a chronic anteroseptal infarct has a low arrhythmogenic potential in pigs. In this model the peri-infarction zone shows a band of sympathetic and parasympathetic denervation secondary to the necrosis.

Animals↗
PubMed1992

Reperfusion arrhythmias after chronic regional denervation of the ischaemic myocardium in pigs.

OBJECTIVE: The aim was to assess the effects of chronic regional denervation of the ischaemic myocardium on reperfusion arrhythmias in a model with sparse coronary collateral circulation. METHODS: Baseline ventricular refractoriness and epicardial activation times were measured together with reperfusion arrhythmias after 15 min (I-15') or 30 min (I-30') of left anterior descending coronary artery occlusion in 38 barbiturate anaesthetised open chest pigs. Twenty pigs (11 in I-15' and nine in I-30') had a chronic (two week) denervation of the left anteroseptal region, whereas 18 pigs (10 in I-15' and eight in I-30') were sham operated (non-denervated) controls. Denervation was induced by pericoronary application of phenol and verified by absence of adrenergic histofluorescence. RESULTS: As compared with controls, denervated pigs showed: (1) longer activation times: 20.3 (SD 5.2) ms v 16.5 (4.6) ms, p < 0.001; (2) slightly longer refractory periods: 348(28) ms v 334(27) ms; (3) a tendency to lower postreperfusion ectopic activity: ectopic beats divided by time free of ventricular tachycardia: 0.13(0.19) v 0.34(0.40) in I-15', and 0.21(0.24) v 0.39(0.44) in I-30'; (4) slower ventricular tachycardia in I-30': 140(29) beats.min-1 v 185(29) beats.min-1, p < 0.009; and (5) comparable incidence of postreperfusion ventricular fibrillation: 4/11 pigs v 2/10 in I-15', and 5/9 v 4/8 in I-30'. CONCLUSIONS: Selective chronic denervation of the ischaemic myocardium was unable to protect against malignant reperfusion arrhythmias in hearts with human-like coronary collaterals. This was confirmed at two ischaemic periods known to produce progressive catecholamine accumulation and increased adrenoceptor density in the ischaemic myocardium.

Animals↗
PubMed1992

T-Q, S-T segment mapping and hyperemia in reperfused pig heart with ischemic preconditioning.

The effects of ischemic preconditioning on epicardial T-Q and S-T segment mapping, local activation, and coronary blood flow were analyzed in nine barbiturate-anesthetized pigs during four coronary occlusion (5 min)-reperfusion (20 min) sequences. In seven sham pigs, one occlusion was performed after a control period of 75 min. The first reperfusion induced a marked coronary hyperemia [11 +/- 4 ml/min (baseline) to 33 +/- 16 ml/min, P < 0.005] and a rapid recovery (30 to 150 s) of epicardial activation delays, T-Q segment depression, and S-T segment elevation in the ischemia area. This recovery was transiently associated with enlargement of intersite T-Q potential variability (alpha: 2.5 +/- 0.6 to 3.4 +/- 0.7 mV, P < 0.05), T-Q segment overshoot to +1.4 +/- 0.9 mV, and S-T segment reelevation. A brief T-Q segment depression (-2.3 +/- 0.9 mV) occurred during early reperfusion in 60 of 91 electrodes overlying the normal myocardium. Compared with the first, the fourth occlusion induced lower S-T segment elevation (3.4 +/- 2.0 to 1.7 +/- 1.9 mV, P < 0.05), and the fourth reperfusion elicited a faster reversal of T-Q segment dispersion (53 +/- 21 to 43 +/- 16 s, P < 0.05), S-T segment elevation (149 +/- 101 to 81 +/- 45 s, P < 0.05), and coronary hyperemia (8 +/- 2 to 5 +/- 1 min, P < 0.05). This trend of changes was not observed during a fourth occlusion in sham pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Reperfusion arrhythmias in isolated perfused pig hearts. Inhomogeneities in extracellular potassium, ST and TQ potentials, and transmembrane action potentials.

We recorded direct current electrograms and local [K+]o at multiple sites and transmembrane potentials at selected sites during reperfusion after 5 minutes and 10 minutes of regional ischemia in isolated perfused pig hearts. After 10 minutes of ischemia, the incidence of ventricular fibrillation (VF) was 38%. At 80-90 seconds after reperfusion, [K+]o was 0.8 mM less than in normal tissue in half of the reperfused tissue, especially in the border zone. This was associated with TQ elevation of +4.5 mV and large peaked T waves. The latter was caused by an abrupt decrease of action potential duration in reperfused tissue, leading to a difference of up to 165 msec with normal tissue. Reperfusion VF started with a closely coupled ventricular premature beat. Activation block between reperfused and normal tissue permitted reentrant activation, leading to VF. Pretreatment with ryanodine (10(-6) M) and reperfusion with elevated [K+] (both of which prevent delayed afterdepolarizations) did not prevent closely coupled ventricular premature beats or VF. Five minutes of ischemia never caused VF. K+ depletion and TQ elevation in the reperfused zone was less frequent and smaller (-0.4 mM and 1.8 mV, respectively). Peaked T waves did not occur, and shortening of the action potential duration was less. We conclude that extracellular K+ depletion and marked action potential duration shortening in the reperfused tissue play a role in the genesis of reperfusion VF, which is caused by reentry. The closely coupled ventricular premature beat that initiates reentry is not caused by delayed afterdepolarizations but most likely by intramural reentry.

Action Potentials↗
PubMed1991

Induced ventricular arrhythmias in regionally denervated porcine heart with healed myocardial infarction.

STUDY OBJECTIVE: The aim was to test the hypothesis that chronic sympathetic denervation of the boundaries of a healed myocardial infarction may modify the arrhythmogenic response to programmed electrical stimulation. DESIGN: Electrical induction of ventricular arrhythmias and infarct size were evaluated in a control group of pigs with a one month old myocardial infarction induced by ligature of the left anterior descending coronary artery below the first diagonal branch. These were compared with a group of similarly infarcted pigs subjected to regional denervation of the peri-infarction area induced by topical pericoronary application of phenol. Denervation was verified by the absence of adrenergic histofluorescent reaction to glyoxylic acid in myocardial samples. EXPERIMENTAL MATERIAL: 24 pigs (weight 15-20 kg) with myocardial infarction were studied, 13 of which were subjected to regional peri-infarction denervation, and 11 acted as controls. MEASUREMENTS AND MAIN RESULTS: Programmed ventricular stimulation with one to four extrastimuli at 500 and 400 ms basic cycle length at the left and right ventricles induced fewer episodes of ventricular fibrillation in the denervated than in the non-denervated group (five episodes in three pigs v 14 in nine pigs, p less than 0.005), but more episodes of sustained ventricular tachycardia (79 in eight pigs v 23 in two, p less than 0.001). Unlike fibrillation, induction of ventricular tachycardia increased with multiple extrastimuli and with short basic cycle length. The denervated preparations tended to develop smaller infarcts but this difference was not statistically significant: infarct weight (g) relative to total ventricular mass (g) = 7.2 (SD 2.4)% v 10.5(4.5)%. CONCLUSIONS: Neural integrity of the non-ischaemic myocardium bordering a healed infarction modulates inducibility of ventricular tachycardia and fibrillation during programmed ventricular stimulation.

Animals↗
PubMed1990

Clinical and electrophysiologic findings in acute ischemic intraHisian bundle-branch block.

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.

Bundle of His↗
PubMed1990

Effects of anaesthesia on acute ischaemic arrhythmias and epicardial electrograms in the pig heart in situ.

STUDY OBJECTIVE: The aim of the study was to assess the influence of general anaesthesia on electrocardiographic and arrhythmogenic responses to left anterior descending coronary artery occlusion. DESIGN: Pigs weighing 18-20 kg were anaesthetised with alpha chloralose 100 mg.kg-1 (n = 9) or thiopentone 30 mg.kg-1 (n = 9) and the arrhythmogenic effects of coronary artery occlusion were examined by sequential electrocardiographic measurements every 5 min and arrhythmia analysis every minute over a 60 min period. RESULTS: alpha Chloralose predisposed to lower ST segment elevation (analysis of variance for repeated measurements p less than 0.002), less marked epicardial conduction delay (p less than 0.01) with slower progression to monophasic potentials, and in contrast, to a greater number of episodes of ventricular premature beats (p less than 0.005), ventricular tachycardia (51 v 32 episodes), and ventricular fibrillation (6 v 2 pigs) than barbiturate anaesthesia. CONCLUSIONS: alpha Chloralose and barbiturates exerted opposite electrocardiographic and arrhythmogenic effects in a porcine model of acute myocardial ischaemia. Due to its proarrhythmic effect chloralose should probably be used in studies dealing with spontaneous and induced ischaemic arrhythmias.

Anesthesia, General↗
PubMed1990

Circadian variations of electrical properties of the heart.

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.

Adolescent↗
PubMed1989

Ventricular arrhythmias and local electrograms after chronic regional denervation of the ischemic area in the pig heart.

Cardiac denervation has been proved to reduce the incidence of coronary occlusion arrhythmias in digs, but the effect of limiting the extent of sympathectomy to the ischemic area, particularly in hearts with sparse coronary collateral circulation, as in the human heart, needs further investigation. Ventricular arrhythmias and changes in epicardial direct current electrograms induced during acute left anterior descending coronary artery occlusion were recorded in 14 pigs subjected to regional denervation of the ischemic area 2 weeks before; these were compared with findings in 14 sham-operated control pigs. Regional denervation was induced by pericoronary application of phenol above the occlusion site and it was confirmed by the loss of myocardial catecholamine histofluorescence. During 35 min of ischemia, significant differences in occurrence of ventricular premature beats, ventricular tachycardia, ST segment elevation, TQ segment depression and epicardial activation delays were observed between the two groups of experiments, with lower values of each variable in the denervated hearts. Ventricular fibrillation occurred 32 times in 11 control pigs and only 15 times in eight denervated hearts. In contrast, programmed ventricular extrastimuli delivered during 35 to 50 min of ischemia induced 39 fibrillatory episodes in 13 denervated hearts and only 14 episodes in seven control pigs. Thus, denervation limited to the ischemic area in hearts with a human-like coronary artery pattern was associated with a decrease in the magnitude of early ischemic arrhythmias and electrocardiographic alterations, but the procedure was unable to prevent early induction of ventricular fibrillation.

Animals↗
PubMed1989

Nocturnal angina in patients with fixed coronary stenosis. Increased coronary vasoconstrictive sensitivity with independence of pacing ischaemic threshold.

Atrial pacing and ergonovine tests were performed in 18 consecutive patients with unstable angina at rest and significant coronary artery stenosis (greater than or equal to 90% in greater than or equal to one vessel in 16 patients). 13 of them also had exertional angina. 14 patients presented at least one positive response (greater than or equal to 1.0 mm ST-segment shift) to pacing, with a heart rate (144 +/- 11 vs 75 +/- 13 beats min-1, P less than 0.001) and double product (195 +/- 26 vs 108 +/- 32 x 10(-2), P less than 0.001) significantly higher than during angina at rest. In the ten patients who presented nocturnal angina, the incidence of positive response to pacing and the pacing ischaemic threshold, tested on three different days, were similar to those seen in the remaining patients. In contrast, the ergonovine test was positive in all patients with nocturnal angina (100%), who required a low dose (0.28 +/- 0.2 mg), but it was positive in only four (50%) of those without nocturnal angina, who needed a higher dose (0.55 +/- 0.12 mg, P less than 0.005). Therefore, in patients with severe coronary stenosis and exertional angina, spontaneous episodes, including nocturnal angina, are not related to increases in heart rate. The increased coronary vasoconstrictive sensitivity found in these patients, particularly those with nocturnal angina, was not dependent on the status of the coronary reserve, which strongly suggests that changes in coronary tone, focal or diffuse, are involved in the mechanisms of these ischaemic events.

Aged↗
PubMed1989

[Intravenous streptokinase in acute myocardial infarction. Reduction of early in-hospital mortality].

A randomized study of the effects of intravenous streptokinase was performed in 214 patients with an acute myocardial infarction of less than 4 hours of whom 110 were included in the therapeutic group (SK) and 104 in the control group (C). Incidence of angiographic recanalization was higher in SK group (71 vs 28%, p less than 0.001) as that of non-significant residual coronary artery stenosis (less than 70%, 16% vs 3%, p less than 0.005), particularly in young patients (less than 45 years; 42% vs 8%, p less than 0.05). However, SK group presented a higher incidence of severe residual stenosis (90-99%) (SK, 42% vs C, 22%, p less than 0.01). Ejection fraction was higher among recanalized patients in both groups. Peak CPK-MB occurred earlier in SK group (13 vs 19 hours, p less than 0.001) and also among the recanalized patients of each group (SK, 12 vs 16 hours, p less than 0.001; C, 15 vs 21 hours, 0.002). The course of ST segment was similar in the 2 groups. The occurrence of ventricular arrhythmias within the first hour was greater in SK group (40% vs 20%, p less than 0.002), whereas the incidence of pericarditis (14% vs 35%, p less than 0.001) and of early mortality (less than 5 days, 2% vs 10%, p less than 0.02) was lower in SK group. The incidence of cardiac rupture, confirmed at necropsy in each of the 5 cases studied, was also lower in SK group (1 vs 8).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Octapolar electrocatheter for His bundle recording and sequential bedside electrophysiologic testing.

To reduce the number of electrocatheters required for an electrophysiologic study and to facilitate prolonged monitoring of the electrical properties of the heart, an octapolar electrocatheter was designed and tested in 45 consecutive patients undergoing routine electrophysiologic studies. The electrocatheter introduced into the right ventricle served for: (a) right ventricular pacing; (b) recording of low lateral and low septal right atrial electrograms; (c) recording of the His bundle potential in 39 out of the 45 patients (86%); (d) 24-hour monitoring of the AV conduction intervals and refractory periods at the patients' bedsides. The octapolar electrocatheter reduced the number of probes required for studying the mechanisms of reciprocating tachycardia and allowed 24-hour bedside electrophysiologic monitoring.

Adult↗