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Biomedical subjects

L Mont

Publications and source records attributed to L Mont.

At least 55 records · Page 3Linked to original sources

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↗

Limitations of head-up tilt test for evaluating the efficacy of therapeutic interventions in patients with vasovagal syncope: results of a controlled study of etilefrine versus placebo.

OBJECTIVES: This study assessed the efficacy of oral etilefrine (10 mg three times a day) in preventing a positive response to head-up tilt testing. BACKGROUND: Previous reports have suggested that oral etilefrine can be effective either in preventing a positive response to head-up tilt testing or in reducing syncopal recurrences in patients with vasovagal syncope. Up to now most studies assessing drug therapy in these patients have been uncontrolled. METHODS: This was a randomized double-blind crossover study of etilefrine versus placebo in 30 consecutive patients with syncope and a baseline positive head-up tilt test. After the first test, patients had no treatment for 3 days and were randomized to receive etilefrine or placebo for 4 additional days. They underwent tilt testing under treatment and again after 3 days of washout; they then received the alternative treatment for 4 days, and a third test was performed. RESULTS: Head-up tilt test results were negative in 13 (43%) patients with etilefrine and 15 (50%) with placebo (p = NS). Therefore, the statistical power of the study was only 10%. The rate of positive responses decreased with repeated testing irrespective of the assigned treatment: A positive response was obtained during the second head-up tilt test in 20 patients (10 with placebo, 10 with etilefrine) but in only 12 during the third (7 with etilefrine, 5 with placebo) (p < 0.05). CONCLUSIONS: Oral etilefrine (10 mg three times a day) was not superior to placebo in preventing a positive response to head-up tilt testing. Despite a low statistical power, the high rate of negative response with placebo (50%) suggests that controlled trials are needed to assess the real efficacy of any treatment in patients with vasovagal syncope.

Administration, Oral↗

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↗

Anatomic, electrical, and mechanical factors affecting bipolar endocardial electrograms. Impact on catheter ablation of manifest left free-wall accessory pathways.

BACKGROUND: The use of bipolar endocardial electrogram characteristics to guide radiofrequency (RF) current catheter ablation of accessory pathways (APs) has been advocated by several investigators. However, the influences of a varying anatomy of the AP and the atrioventricular groove, of different ablative approaches, and of RF current pulses preceding the final pulse have not been adequately addressed. METHODS AND RESULTS: Local bipolar endocardial electrograms were retrospectively analyzed in a uniform cohort of 62 consecutive patients with a single manifest AP located on the left free wall; in all patients, the AP had been ablated by a uniform approach with a single catheter advanced retrogradely toward the mitral annulus. Electrogram parameters assessed were the presence or absence of a presumed AP potential, the atrial-to-ventricular (A/V) amplitude ratio, the A-V interval, and the onset of delta wave to local ventricular activation (delta-V) interval. The AP location was classified on fluoroscopy as anterior, lateral, or posterior. Catheter stability was verified by comparing pre- and post-RF amplitudes of local atrial potentials. The ablation site was ventricular in 52 patients (group A) and atrial in 10 (group B). In group A, 26 APs (50%) required a single RF current pulse for ablation. These APs showed no anatomic predilection and no statistically significant differences in electrogram parameters from 24 APs that were ablated only after a median of three pulses had failed, suggestive of a wider ventricular insertion of the latter APs. A lower A/V ratio and a higher incidence of transient AP block found in the remaining 2 group A patients, who had anteriorly located APs requiring > 10 failed pulses, suggested an adverse anatomy of the A-V groove in that region. A stepwise multivariate logistic regression analysis revealed that the simultaneous presence of (1) a presumed AP potential, (2) an A/V ratio > or = 0.10, (3) an A-V interval < or = 40 milliseconds, and (4) a delta-V interval < or = 0 milliseconds was associated with a specificity of 94% and a positive predictive accuracy of 87% for an RF pulse to be successfully applied to the ventricular insertion to the AP. Compared with APs of group A, APs of group B were distinguished by unsuccessful ventricular pulses associated with a delta-V interval > 10 milliseconds in the presence of an A/V ratio > 0.33 (specificity of 97% and positive predictive accuracy of 82%), which is suggestive of a more epicardial ventricular insertion of these APs. CONCLUSIONS: The effect of anatomic variations of the AP and the A-V groove is reflected in the bipolar endocardial electrogram and needs to be considered in the approach to AP ablation. The stepwise inclusion of the four electrogram criteria introduced in this study may improve the efficacy of RF catheter ablation of a manifest left free-wall AP at its ventricular insertion. Whenever mapping cannot improve on a delta-V interval > 10 milliseconds despite apparently close contact with the mitral annulus ("good" A/V ratio), attempts at ablation are likely to be successful at the atrial aspect of the mitral annulus.

Adult↗

[The predictors of success in the radiofrequency ablation of left accessory pathways using the single-catheter technic].

INTRODUCTION AND OBJECTIVES: To determine the predictors of successful radiofrequency current ablation of an accessory pathway using the single-catheter approach, we retrospectively analyzed 46 consecutive patients with left sided accessory atrioventricular pathways and manifest preexcitation. METHODS: Ablation using a single catheter advanced retrogradely towards the mitral valve was successful in 42 (91%). A radiofrequency pulse resulting in permanent accessory pathway block was defined as a successful pulse; a pulse that had no effect or caused only transient accessory pathway block was defined as an unsuccessful pulse. RESULTS: Successful radiofrequency pulses (n = 37) did not differ from those that failed (n = 56) in the local atrium-accessory pathway potential interval, in the accessory pathway-ventricle interval nor in the cumulative energy delivered. But in successful radiofrequency pulses, the amplitude ratio of local atrium and ventricular potentials tended to be larger (0.29 +/- 0.17 vs 0.23 +/- 0.17; p = 0.053) and presumed accessory pathway potential was more often recorded (36 [97%] vs 38 [68%]; p = 0.006). The time elapsed from the beginning of the current application and the accessory pathway block was shorter in successful pulses as compared to those pulses producing only transient block (3.3 +/- 2 s vs 6.9 +/- 4 s). CONCLUSIONS: The recording of a presumed accessory pathway potential, a large local A/V ratio and the occurrence of early conduction block in the accessory pathway were the best predictors of successful radiofrequency current application using the single-catheter approach.

Adolescent↗

Incidence, pathophysiology and prognosis of exercise-induced sustained ventricular tachycardia associated with healed myocardial infarction.

Of 150 consecutive patients with sustained monomorphic ventricular tachycardia (VT) (n = 116) or ventricular fibrillation (VF) (n = 34) late after acute myocardial infarction, 17 had reproduction of their sustained monomorphic VT during exercise testing. Data from these patients (group I) were compared with data from patients without exercise-induced VT (group II). No statistical difference was found between groups I and II with relation to age, sex, number of vessels with greater than 70% stenosis, left ventricular ejection fraction, number of previous myocardial infarctions, inducibility during programmed stimulation and total mortality during follow-up. In group I, only 1 patient (6%) developed ST depression during exercise compared with 47 patients (35%) in group II (p less than 0.01). After a 34-month mean follow-up, 6 patients in group I (35%) and 18 patients in group II (13%) died suddenly (p = 0.02). It is concluded that sustained monomorphic VT is reproduced during exercise in only 11% of patients with spontaneous late sustained monomorphic VT or VF. Electrocardiographic findings do not support ischemia as a triggering mechanism of exercise-induced sustained monomorphic VT. Patients with exercise-induced sustained monomorphic VT have a high incidence of sudden death.

Coronary Angiography↗

The electrocardiographic, clinical, and electrophysiologic spectrum of idiopathic monomorphic ventricular tachycardia.

Clinical, ECG, and electrophysiologic data from 47 patients who had episodes of sustained or nonsustained monomorphic VT with no evidence of structural heart disease were reviewed. According to the QRS configuration during tachycardia, four groups were distinguished. Nine patients had a right bundle branch block configuration and superior frontal plane QRS axis (group 1). Nine patients had a right bundle branch block configuration but an intermediate or right QRS axis (group 2). Group 3 consisted of five patients with a left bundle branch block configuration and a left axis deviation, and in group 4 there were 24 patients who had a left bundle branch block configuration with an intermediate or right frontal axis. Patients in group 1 had dizziness during tachycardia less frequently, but they needed cardioversion to terminate their arrhythmias more often. They experienced tachycardia during exercise less often, and tachycardia was not initiated during exercise testing. They had fewer ventricular premature beats according to the Holter recording. During the electrophysiologic study, VT was induced and terminated by pacing more often in this group. Patients with idiopathic VT with a right bundle branch block configuration and a superior axis seem to be a unique group of patients with idiopathic VT, and reentry seems to be the most likely arrhythmia mechanism in this group. The other ECG configurations share the same clinical and electrophysiologic characteristics, which suggest that the underlying arrhythmia mechanism is the same.

Adult↗

Clinical and electrophysiologic characteristics of exercise-related idiopathic ventricular tachycardia.

In 37 (70%) of 53 patients with idiopathic ventricular tachycardia (VT), episodes were mainly related to exercise (group 1). These patients were younger (33 +/- 14 vs 44 +/- 18 years, p = 0.015) and more often had dizziness during VT (71 vs 40%, p = 0.003) than the 16 patients in whom VT was not exercise-related (group 2). Patients in group 1 needed cardioversion less often to terminate the arrhythmia (4 (11%) vs 6 (40%), group 2 [p = 0.04]). VT was initiated during exercise testing in 62% of patients in group 1 but in only 1 patient in group 2 (p = 0.0004). Induction of clinical VT during programmed stimulation was observed in a similar percentage in group 1 (49%) and group 2 (50%) patients. Isoproterenol infusion facilitated the induction of VT in 9 of 20 (45%) group 1 and in 2 of 8 (25%) group 2 patients (p = not significant). After a mean follow-up of 2.9 +/- 2.5 years, 8 (22%) group 1 patients and 5 (31%) group 2 had at least 1 episode of symptomatic VT. Only 1 patient died suddenly. Class III drugs were the most useful in preventing recurrences. Beta-blocking agents were of little value in both groups. Patients with VT and a structurally normal heart have a good prognosis despite recurrences of their arrhythmia. The relation of the arrhythmia to exercise has no prognostic implications.

Adult↗

On the mechanisms of ventricular tachycardia acceleration during programmed electrical stimulation.

BACKGROUND: The pathophysiological mechanisms leading to acceleration of ventricular tachycardia (VT) are still unclear. METHODS AND RESULTS: High-resolution epicardial mapping was used to study the mechanisms of VT acceleration by programmed electrical stimulation (PES) in a model of sustained reentrant VT in Langendorff-perfused rabbit hearts (n = 40). Three different mechanisms responsible for acceleration of VT were identified: 1) induction of double-wave reentry (n = 6), defined as the occurrence of two successive activation waves circulating in the same direction in the same circuit; 2) change to a functionally determined circuit (n = 4), defined as reentry of the impulse around a functional line of block without involvement of a fixed obstacle; and 3) change of the reentrant circuit to reentry within a different, faster anatomic pathway (n = 3). Analysis of 81 episodes of sustained monomorphic VT induced by PES in 74 patients with clinically documented sustained VT in the setting of chronic coronary artery disease showed that in 22 episodes VT was suddenly accelerated by PES (mean cycle length, from 345 +/- 73 to 277 +/- 71 msec, p less than 0.01). CONCLUSIONS: With the observations made in the experimental model, the following tentative classification of the mechanisms of VT acceleration of the 22 episodes was made: 1) induction of double-wave reentry in two, 2) change to a functionally determined circuit in four, and 3) change to reentry within a faster anatomic circuit in 16. Simple criteria suggest that these mechanisms may apply in the clinical situation.

Animals↗

A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.

BACKGROUND: In the differential diagnosis of a tachycardia with a wide QRS complex (greater than or equal to 0.12 second) diagnostic mistakes are frequent. Therefore, we investigated the reasons for failure of presently available criteria, and we identified new, simpler criteria and incorporated them in a stepwise approach that provides better sensitivity and specificity for making a correct diagnosis. METHODS AND RESULTS: A prospective analysis revealed that current criteria had a poor specificity for the differential diagnosis. The value of four new criteria incorporated in a stepwise approach was prospectively analyzed in a total of 554 tachycardias with a widened QRS complex (384 ventricular and 170 supraventricular). The sensitivity of the four consecutive steps was 0.987, and the specificity was 0.965. CONCLUSIONS: Current criteria for the differential diagnosis between supraventricular tachycardia with aberrant conduction and ventricular tachycardia are frequently absent or suggest the wrong diagnosis. The absence of an RS complex in all precordial leads is easily recognizable and highly specific for the diagnosis of ventricular tachycardia. When an RS complex is present in one or more precordial leads, an RS interval of more than 100 msec is highly specific for ventricular tachycardia. This new stepwise approach may prevent diagnostic mistakes.

Diagnosis, Differential↗

Differential effects of heptanol, potassium, and tetrodotoxin on reentrant ventricular tachycardia around a fixed obstacle in anisotropic myocardium.

BACKGROUND: The aim of this study was to test the hypothesis that electrical uncoupling and depression of the fast sodium channels have differential effects on propagation of the electrical impulse relative to the fiber orientation. METHODS AND RESULTS: In a model of reentrant ventricular tachycardia (VT) (mean cycle length, 144 +/- 13 msec) around a ring of anisotropic myocardium in 10 Langendorff-perfused rabbit hearts, the effects of extracellular K+ concentration [( K+]o) and heptanol were studied. [K+]o and heptanol each had a dose-dependent effect on VT cycle length. However, high [K+]o slowed the VT mainly by depressing longitudinal conduction, whereas heptanol preferentially depressed transverse conduction. The ratio between longitudinal and transverse conduction velocities progressively decreased with high [K+]o and progressively increased with heptanol. Heptanol terminated VT at a mean concentration of 3.5 +/- 0.5 mM. The cycle length before termination was 446 +/- 120 msec (p less than 0.001). In eight of 10 experiments, termination occurred by failure of conduction during transverse propagation. VT terminated at a mean [K+]o of 11.6 +/- 1.8 mM. The cycle length before termination was 493 +/- 341 msec (p less than 0.01). In seven of 10 cases, termination occurred by failure of conduction during longitudinal propagation. In the remaining five episodes (two with heptanol and three with high [K+]o), termination occurred by collision of the reentrant beat with an antidromic impulse being reflected within the ring. In a separate series of six hearts, tetrodotoxin was administered during VT. Like high [K+]o, tetrodotoxin prolonged the cycle length of the VT by preferentially slowing longitudinal conduction, and VT was terminated by longitudinal block. CONCLUSIONS: During reentrant VT, electrical uncoupling of cells by heptanol or modification of active membrane properties by high [K+]o or tetrodotoxin has a differential depressing effect on propagation of the impulse relative to the fiber orientation.

Alcohols↗

Mechanisms of sudden cardiac death.

Although coronary artery disease is the most frequent cause of sudden cardiac death, it may be caused by a heterogeneous group of disorders. Acute ischaemia is responsible for about half the cases of sudden death after acute myocardial infarction, and is manifested through ventricular fibrillation or polymorphic ventricular tachycardia. Several factors affect the haemodynamic consequences of a ventricular arrhythmia. Re-entry is the mechanism involved in patients with a history of myocardial infarction and therapy should be individualised and directed to the arrhythmia. Simple decision trees are available that can help to find the most appropriate therapy; implantable defibrillators are the most effective modality in certain very high risk subsets.

Arrhythmias, Cardiac↗

Does left ventricular aneurysm influence survival after acute myocardial infarction?

To test whether left ventricular aneurysm independently influences survival after acute myocardial infarction, a series of 386 consecutive men aged 60 years or less, were followed up for 57 (40-100) months. Catheterization was performed 1 month following the infarct. Aneurysm, defined as a diastolic outward bulging with akinetic or dyskinetic systolic motion, was diagnosed in 52 patients (13.5%). Mortality was higher (29% vs 14%; P less than 0.02) in patients with left ventricular aneurysm; their probability of survival at 60 months was 75% vs 90% in patients without aneurysm. Cox regression analysis for the whole population identified ejection fraction, bifascicular block, number of diseased vessels and angina after infarction as the only independent predictors of survival; when adjusted for these variables, differences in mortality between patients with and without aneurysm were no longer significant. To investigate further the role of aneurysm in survival, the 52 patients presenting with left ventricular aneurysm were matched with 52 of the remaining 334 patients according to the following baseline variables: ejection fraction, number of diseased vessels, left ventricular end-diastolic pressure, and bifascicular block. The survival curves of these two subsets were similar (mortality rates of 75% and 82%, respectively). Cox regression analysis of the whole cohort of 104 patients selected bifascicular block and the number of diseased vessels, but not left ventricular aneurysm, as independent predictors of outcome.

Follow-Up Studies↗

The effects of alcoholism on skeletal and cardiac muscle.

To determine the prevalence of alcoholic myopathy and cardiomyopathy, we studied a group of 50 asymptomatic alcoholic men (mean age, 38.5 years) entering an outpatient treatment program. Studies performed included an assessment of muscle strength by electronic myometer, muscle biopsy, echocardiography, and radionuclide cardiac scanning, with comparison to healthy control subjects of similar age. The patients' mean (+/- SEM) daily alcohol consumption was 243 +/- 13 g over an average of 16 years. These patients had no clinical or laboratory signs of malnutrition or electrolyte imbalance. Forty-two percent of the patients, as compared with none of the controls, had strength of less than 20 kg as measured in the deltoid muscle. Muscle-biopsy specimens from 23 patients (46 percent) had histologic evidence of myopathy. In the cardiac studies, when the alcoholic patients were compared with 20 healthy controls, the patients had a significantly lower mean ejection fraction (59 vs. 67 percent), a lower mean shortening fraction (33 vs. 38 percent), a greater mean end-diastolic diameter (51 vs. 49 mm), and a greater mean left ventricular mass (123 vs. 106 g per square meter of body-surface area). One third of the alcoholics had an ejection fraction of 55 percent or less, as compared with none of the controls. Endomyocardial biopsy specimens from six patients with ejection fractions below 50 percent showed histologic changes of cardiomyopathy. The estimated total lifetime dose of ethanol correlated inversely with muscular strength (r = -0.65; P less than 0.001). In an analysis that also included six patients with symptomatic alcoholic cardiomyopathy, the estimated total lifetime dose of ethanol correlated inversely with the ejection fraction (r = -0.58; P less than 0.001) and directly with the left ventricular mass (r = 0.59; P less than 0.001). We conclude that myopathy of skeletal muscle and cardiomyopathy are common among persons with chronic alcoholism and that alcohol is toxic to striated muscle in a dose-dependent manner.

Adult↗

[Reversibility of alcoholic myocardiopathy with abstinence: presentation of 2 cases].

The sustained alcohol intake results in the development of a dilated cardiomyopathy; its pathogenesis and prognostic and evolutive factors have not yet been completely defined. It is classically considered that alcoholic cardiomyopathy has a poor prognosis, as two thirds of patients die within three years. However, in recent years some isolated cases of clinical reversibility after short abstinence periods have been reported without identification of the involved factors. Two chronic alcoholic patients are reported with congestive heart failure at admission; a diagnosis of alcoholic cardiomyopathy was made after cardiac catheterization and endomyocardial biopsy. The morphometric study of endomyocardial biopsy showed a preservation of the myofibrillary fraction with mild fibrosis. The clinical outcome was favorable: after three months of alcoholic abstinence, a complete clinical recovery with definite improvement of echocardiographic parameters and left ventricular ejection fraction in the radionuclide ventriculography were observed. Finally, the factors that appear to be involved in the presence or absence of reversibility of this type of cardiomyopathy are discussed.

Adult↗