Biomedical subjects

D A Sideris

Publications and source records attributed to D A Sideris.

At least 19 recordsLinked to original sources

PubMed1995

Incidence and other epidemiological characteristics of sudden cardiac death in northwest Greece.

Sudden cardiac death (SCD) has not been investigated separately in Greece. The aim of this study is to describe the epidemiological characteristics of people dying suddenly out of hospital in an area of Greece. In 1990, a population based study was started to detect the cases of people dying suddenly out of hospital (< 1 h after onset of acute symptoms or < 6 h after being seen alive) in a closed population in Northwest Greece (Ioannina area: 160,000 inhabitants). During a 3.5 year period, 283 potential cases aged 30-70 years were identified by monitoring the mortality in the emergency rooms of the two hospitals of the area, the coroner's office and the death certificates from the Government Department of Statistics. The diagnosis of SCD was established in 223 (183 men, 40 women; mean ages 59 and 61 years respectively) after visiting and interviewing the relatives and/or the family doctors within 12 days (range 1-28) after the death. SCD in the study accounts for 50% of all cardiovascular deaths and is the most common cause of death after neoplasia. The most common place of death was home (151 cases, 68%), and in 174 cases (78%) deaths occurred while the patients were relaxing or during routine activities. Prodromal symptoms were reported in 57 cases (26%). The time of day of death showed a circadian variation, with a peak in the late morning from 9:00 to 12:00. Ninety four (42%) had a prior history of heart disease. One hundred and ninety one cases (86%) occurred in the subgroup of age 50-70 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Effect of preload and afterload on ventricular arrhythmogenesis.

To examine whether it is an increase in preload or afterload that may cause ventricular arrhythmias, the ventricles of 13 anesthetized open-chest dogs were bandaged. Next, metaraminol, an almost pure alpha stimulator, was given, followed by removal of the bandage. The ventricles were then sucked in a plastic cup, which was finally removed. The systolic and diastolic ventricular pressures were measured, and the presence of arrhythmias (ventricular ectopic beats or ventricular tachycardia) was observed. Banding the ventricles caused a significant diminution of systolic pressure (-42 +/- 38.0 mmHg; mean +/- SD) and a rise in diastolic pressure (+3.5 +/- 3.7), starting from control values of 126 +/- 36/6.5 +/- 3.0, but no arrhythmia. Metaraminol raised both pressures (+122 +/- 58 and +9.0 +/- 10.3) and caused ventricular arrhythmias in 6 of 13 experiments. Removing the bandage further increased the systolic pressure (+45 +/- 42) and reduced the diastolic pressure (-7.2 +/- 10.3), but made the arrhythmia worse in 10 of 13 experiments. Suction reduced both pressures (-166 +/- 96 and -5.4 +/- 14) and stopped all arrhythmias. Removing the cup increased both pressures (+133 +/- 68 and +15.5 +/- 15.3, respectively) and worsened the arrhythmia in seven of eight experiments. In general, deterioration of ventricular arrhythmias was observed in 23 of 25 maneuvers with either an increase or no change in systolic pressure, but in none of the maneuvers was there a decrease (P < .0001) in systolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Cardiac involvement in collagen diseases.

The purpose of this study is to evaluate the early morphological and functional abnormalities of the heart in patients with collagen disease. The study population was free of risk factors for coronary artery disease and without any clinically evident cardiac manifestations. In 62 patients with collagen disease (25 with progressive systemic sclerosis, 19 with systemic lupus erythematosus, 15 with rheumatoid arthritis, three with dermatomyositis) and in 40 healthy subjects an echocardiographic study was performed. Echocardiographic examination from the apical four-chamber view was performed at rest and during the end of a 3 min isometric exercise with handgrip. Global and regional ejection fraction of the left ventricle were calculated. In the group with progressive systemic sclerosis the left ventricular mass index was significantly higher than in the control group (110.78 +/- 48.61 vs 82.18 +/- 28.46 g.m-2) and the ejection fraction (53.61 +/- 7.95%) was the lowest of all groups (control: 61.47 +/- 8.52%, systemic lupus erythematosus: 59.04 +/- 8.58%, rheumatoid arthritis: 62.38 +/- 6.88%). Regional ejection fraction analysis revealed a major dysfunction of the proximal segment of the interventricular septum, in all groups. During isometric exercise, the global and regional ejection fraction did not change significantly, although differences between groups disappeared. In rheumatoid arthritis, mitral and aortic valve leaflet separation appeared to be reduced. In the group with systemic lupus erythematosus, mild abnormalities were noticed, although the mean age and duration of the disease were the smallest compared with the other groups. In conclusion, patients with progressive systemic sclerosis mainly present left ventricular hypertrophy with a reduced ejection fraction while rheumatoid arthritis patients show a predominant valve dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Atrial pressure and experimental atrial fibrillation.

A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300-600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 +/- 12.2 mmHg, mean +/- SD) than maintenance of sinus rhythm (16.8 +/- 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.

Animals↗

PubMed1994

Effect of acute ventricular pressure changes on QRS duration.

The effect of acute changes in ventricular pressure is examined on the QRS duration to clarify the mechanism of ventricular pressure-related arrhythmogenesis. Ventricular pressure was changed acutely by arterial transfusion-bleeding into an open-air ventricular pressure reservoir that was either off or on a metaraminol intravenous drip. While maintaining ventricular pressure at several levels, the QRS duration was measured at 200 mm/s paper speed. The QRS duration correlated significantly with the left ventricular pressure in all 14 dogs examined. An average change in ventricular by 100 mmHg was associated with a change of about 18% in the QRS duration. An acute ventricular pressure elevation impairs the ventricular conduction, which may contribute to ventricular pressure-related arrhythmogenicity.

Animals↗

PubMed1994

Some observations on the mechanism of pressure related atrial fibrillation.

In order to investigate the effect of atrial pressure on the propensity of the atria to fibrillate and the mechanism of this association, the right atrial pressure was changed acutely by transfusion-bleeding in 12 anaesthetized open-chest dogs. Under various atrial pressures the conduction time was measured between two pairs of hook electrodes positioned on the two atrial appendages respectively. The effective refractory period was measured by continuous pacing of the right atrium at a 250 ms cycle length at double threshold intensity and interpolating a progressively earlier stimulus after each eighth paced beat. The propensity of fibrillation was studied by rapid (450 min-1) pacing of the atria at double threshold intensity for 10 s at different atrial pressures. At a high (> or = 14 mmHg) atrial pressure the conduction time (45.7 +/- 14.2 ms) was significantly (P < 0.01) longer, the effective refractory period (157.9 +/- 15.2 ms) significantly (P < 0.01) longer and the atrial fibrillation (11/19 or 57.9%) significantly (chi 2 = 9.95, P < 0.001) more common than at a low (< or = 10 mmHg) pressure (35.2 +/- 11.6, 146.2 +/- 12.4, 3/24 or 12.5%, respectively). Analysis of variance showed that the probability of atrial fibrillation was significantly affected by the atrial pressure but not by either the conduction time or the effective refractory period. The findings suggest that an increase in right atrial pressure by acute volume overload prolongs the inter-atrial conduction time and right atrial refractoriness and increases the propensity of the atria to fibrillate by rapid atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1994

Acute effects of external and internal pacing on ejection fraction in patients with severe cardiac failure.

The present study aims at evaluating the acute hemodynamic effects of external and internal (3 and 15 mA) pacing on 30 patients with severe cardiac failure. The global and regional ejection fraction were calculated by repeated radionuclide ventriculography at rest (control) and during increasing pacing rates. Blood pressure was measured at the end of each scintigraphy data acquisition period. The pacing rate was increased by 10 beats/min in every step and varied between +10 to +60 beats/min above the resting heart rate. The ejection fraction during pacing was lower than the resting ejection fraction in every pacing mode (resting ejection fraction = 23.30 +/- 7.67%, external pacing = 19.36 +/- 9.30%, p < 0.05, internal pacing 3 mA = 22.15 +/- 7.00%, p = N.S., internal pacing 15 mA = 19.92 +/- 6.95%, p < 0.05). The resting ejection fraction was higher than the ejection fraction in every pacing rate. In 4 out of 30 patients the ejection fraction was higher in every pacing mode and rate than the resting ejection fraction. The regional ejection fraction of the interventricular septum during internal pacing was lower (p < 0.001) than resting and/or external pacing. In conclusion, pacing in patients with severe cardiac failure reduces the control ejection fraction. This reduction increases as the pacing rate increases. The reduction is greater with internal pacing of 15 mA while the hemodynamic effect in external pacing did not differ significantly from internal pacing. Overall, the resting ejection fraction was higher than the paced ejection fraction, although in some patients pacing improved their resting ejection fraction.

Adult↗

PubMed1993

Susceptibility of the right and left canine atria to fibrillation in hyperglycemia and hypoglycemia.

The objective of this study was to investigate the changes in the refractory period and in the susceptibility to fibrillation of canine atria associated with different levels of glycemia, and the differences in these parameters between the two atria. In 20 anesthetized, open-chest dogs weighing 24 kg, the effective refractory period was measured by atrial pacing with a run of 8 stimuli (S1-S1 350 ms) followed by a progressively earlier S2 until no stimulation of the atrial tissue occurred. The susceptibility to fibrillation was assessed by applying DC at 2, 3, and 4 V for 3 seconds, 7 times each, on the atrial appendage. If fibrillation occurred and persisted for 3 minutes, a transthoracic synchronized shock was delivered (200 J). The refractory period and the susceptibility to fibrillation were assessed under normoglycemia first, and then under hypo and hyperglycemia, in the right and left atrium successively, in random order. The incidence of induced atrial fibrillation in the right atrium was: hypoglycemia 31.96% (132 of 413 attempts); normoglycemia 24.11% (81 of 336; p < 0.05); and hyperglycemia 20.23% (85 of 420). Results for the left atrium were hypoglycemia 52.06% (215 of 413); normoglycemia 40.18% (135 of 336; p < 0.005); and hyperglycemia 32.86% (138 of 420; p < 0.05). Sustained atrial fibrillation (> 3 minutes) occurred significantly more often under hypo rather than hyperglycemia and stimulated the left rather than the right atrium. The refractory period was shortest under hypoglycemia in the left atrium and longest under normo or hyperglycemia in the right atrium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Atrial late potentials: paroxysmal supraventricular tachycardia versus paroxysmal atrial fibrillation.

The atrial signal averaged electrocardiogram has been used to detect patients at risk for paroxysmal atrial fibrillation but not yet for paroxysmal supraventricular tachycardia. The P-wave-triggered signal-averaged electrocardiogram, during sinus rhythm, was obtained from 97 subjects divided in groups as follows: 30 controls (Group C), 38 patients with documented paroxysmal atrial fibrillation (Group A) and 29 with documented paroxysmal supraventricular tachycardia (Group B). The atrial duration, root mean square of last 20 and 30 ms and the P-QRS segment were measured. Atrial late potentials were considered to exist when: atrial duration was > 120 ms and root mean square of last 20 ms were < 3.5 microV. The atrial duration (ms) was significantly shorter (P < 0.001) in Group C (113.4 +/- 8) than in Group A (138.5 +/- 23.8) and Group B (134.3 +/- 14.3). The root mean square (microV) of last 20 ms was significantly higher (P < 0.001) in Group C (5.2 +/- 2.5) than in Group A (2.5 +/- 1.3) and Group B (3.1 +/- 1.8). Atrial late potentials were present in 3/30 controls, 32/38 of Group A cases and 23/29 of Group B. The specificity and sensitivity were, respectively: 0.90, 0.84, for Group A, and 0.90, 0.79 for Group B. The P-QRS segment (ms) was significantly shorter (P < 0.01) in Group B (12.5 +/- 9.4) than in Group C (32.5 +/- 16.9) and Group A (20.5 +/- 13.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

High blood pressure and ventricular arrhythmias.

Here we review the blood pressure-ventricular arrhythmia relationship. An increase in blood pressure, by any means, may induce ventricular arrhythmias both experimentally and in patients with a history of ventricular ectopic beats. Conversely, a decrease in blood pressure may eliminate ventricular arrhythmias due to other causes. The increased pressure is sensed in the ventricles. Both systolic and diastolic loading may induce important electrophysiological changes. However, an increase in systolic pressure may induce ventricular ectopy even though the left atrial pressure remains low; on the other hand, raising the atrial pressure does not induce ectopic rhythms unless associated with an increase in arterial pressure. This phenomenon (mechanoelectrical association or contraction-excitation feedback) seems to be a direct one not mediated by either ischaemia or adrenergic stimulation. Both refractoriness and intraventricular conduction are affected by mechanical loading, although the direction of change depends on several factors. The mechanism of pressure-related arrhythmias remains obscure. Triggered activity due to early after-depolarizations is one possibility. Ventricular arrhythmias observed in chronic hypertension might be a clinical manifestation of mechano-electrical association, especially when they occur in conjunction with acute blood pressure elevations. Several antihypertensive agents with different mechanisms of action also have an antiarrhythmic effect. Extensive research to establish the antiarrhythmic effectiveness of antihypertensive treatment in cases with ventricular arrhythmias is still warranted.

Animals↗

PubMed1993

Effect of acute blood pressure changes on signal averaged electrocardiogram.

An acute blood pressure elevation may cause ventricular ectopic rhythms, while its reduction may alleviate them. It is studied whether the blood pressure exerts some effect on parameters obtained by the signal averaged electrocardiogram. In 25 patients with either hypertension (8 cases) or ventricular ectopic rhythms (10 cases) or both (7 cases) the blood pressure was reduced by sodium nitroprusside (24 cases) and/or elevated with metaraminol (10 cases) and the signal averaging electrocardiogram was recorded under 2 or 3 pressure values on each patient. During the high pressure (193.6 +/- 20.1 mm Hg) the following differences were noted compared to the low pressure (77.4 +/- 15.2 less): longer QRS duration in all 25 patients (+9.92 +/- 10.51 ms, P < 0.001); longer low (< 40 microV) amplitude signals (LAS) in 18 patients (+6.94 +/- 10.93 ms, P < 0.005); lower root mean square voltage of the terminal 40 ms of the QRS in 22 patients (-15.73 +/- 21.60 microV, P < 0.005); and ventricular ectopic beat incidence higher in 8, lower in 1, and equal in 2 cases (with no arrhythmia in the other 14). The generally and focally reduced conduction, as suggested by the QRS and LAS prolongation, might contribute to the proarrhythmic effect of acute blood pressure elevation.

Adult↗

PubMed1992

The circadian profile of extrasystolic arrhythmia: its relationship to heart rate and blood pressure.

This paper aims at examining whether there is an association between the circadian patterns of systolic blood pressure, heart rate and the incidence of ventricular ectopic beats, as well as to confirm that reducing the blood pressure by a diuretic may also reduce the ectopic frequency. Thirty-four ambulatory patients with ventricular ectopic beats and a systolic blood pressure of 131.33 +/- 17.46 mmHg had a 24-hour Holter electrocardiographic and blood pressure monitoring following 1 week off any antiarrhythmic and antihypertensive treatment. Then they received for one week a standard diuretic combination (amiloride 5 mg + hydrochlorothiazide 50 mg) at a dose depending on their systolic pressure value and their monitoring was repeated. The mean hourly values of systolic blood pressure, heart rate and ventricular ectopic beats were "normalized", i.e. expressed as (x-x)/SD, taking each patient's 24-hour average as zero and his own standard deviation as the unit of measurement. As a group, there was an independent positive correlation between blood pressure and ectopic beats, while the heart rate was a nonsignificant negative factor for ectopic beats. On an individual level, however, an independent positive significant correlation between blood pressure and ectopic beats was found in only 8 cases, with a negative one in 4 cases. While the blood pressure of the group ranged symmetrically around its daily average value, the corresponding ectopic beat curve was highly asymmetric, with a very high incidence (up to 2.56 +/- 0.52 SD) for a rather short time (only 9.41 +/- 3.56 hours above average) and a low incidence (up to 1.26 +/- 0.49 SD) for the remaining 14.59 hours below average. Sudden rises in ectopic beat (greater than 1 SD/hour) occurred 1 to 6 times per day in each individual, significantly (P less than 0.01) more often (20.31%) with a high (greater than 1 SD) blood pressure than with a low (less than -1 SD) one (8.99%) with intermediate frequencies at intermediate pressures. After treatment with the diuretic, the systolic blood pressure was reduced, the heart rate increased and the ventricular ectopic beat incidence reduced (significant changes). The mean change in systolic pressure in 25 patients with a reduction in ectopy was a significant (P less than 0.01) decrease (-5.21 +/- 8.70 mmHg) while in the remaining 9 cases there was a non significant increase (+1.68 +/- 7.63 mmHg). The heart rate was higher in both subgroups.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1992

Anatomical origin of pressure-related ventricular ectopic rhythms.

In order to determine the origin of pressure-related ectopic rhythms, the main arteries were clamped in 11 anesthetized dogs, or the arteries or veins were transfused, while on or off metaraminol. The epicardial right atrial electrogram, the intracavity electrograms and the pressure of the two ventricles were recorded. Sinus rhythm was associated with 64/64 (100%) of the control periods off metaraminol, but only 19/50 (38%) of the clamping of the main arteries (P << 0.0005). In 14/27 aortic clampings ectopic beats appeared from the left ventricle and in 13/27 from the right one. In 4/23 clampings of the pulmonary artery ectopic beats appeared from the left ventricle and in 15/23 from the right one (P < 0.05). Sinus rhythm was associated with significantly lower left ventricular systolic pressure than any ventricular arrhythmia. The left ventricular systolic pressure associated with ectopic rhythms from the left ventricle was significantly (P < 0.005) higher than that associated with those from the right ventricle. The right ventricular systolic pressure during sinus rhythm was significantly (P < 0.005) lower than that during ectopic rhythm from any ventricle. It is concluded that a rise in the pressure of one ventricle tends to cause ventricular ectopic rhythms originating predominantly, but not exclusively, from this ventricle. The origin of ventricular ectopic rhythms from the right ventricle does not preclude that the arrhythmia may respond favorably to lowering of the systemic pressure.

Animals↗

PubMed1992

Effects of group psychosocial intervention on coronary risk factors.

The purpose of this study was to investigate whether a psychosocial intervention approach aimed at resolving psychological conflicts could reduce the severity of risk factors for post-acute myocardial infarction patients. Twenty-three patients with a recent myocardial infarction participated in a group psychosocial intervention program which lasted 1 year. Twenty other patients with recent myocardial infarction served as controls. Patients form both groups had regular clinical and laboratory follow-up as well as medication. Mean values for seven risk factors of coronary heart disease (smoking, S; body weight, W; serum cholesterol, C; triglycerides, T; systolic and diastolic blood pressure, SBP, DBP; serum uric acid, U) were compared between the two groups in the 1st, 3rd, 6th and 12th months of the follow-up. The maximal mean improvements of the study versus the control group were as follows: W: -2.82 vs. -1.05 kg; C: -56.04 vs. -6.25 mg/dl; T: -20.61 vs. -2.4 mg/dl; U: -0.57 vs. -0.9 mg/dl; S at 1 year -55.5 vs. -10%. It is concluded that group psychosocial intervention with post-acute myocardial infarction patients considerably reduces some coronary-disease risk factors.

Aged↗

PubMed1992

The role of mitral annulus motion in left ventricular function.

The dynamics between mitral annulus motion and left ventricular function were studied. Thirty subjects (10 normals, 10 with severe cardiac failure and 10 with mitral regurgitation) were examined. Left ventricular long and short-axis dimensions were measured in a two-dimensional apical four-chamber image. A volume was calculated as defined by cardiac cyclic changes of mitral annulus in size and motion. This volume had the approximate geometric configuration of a truncuated cone and was covered by mitral annulus motion at enddiastole and endsystole. Left ventricular ejection fraction was calculated echocardiographically using the prolate ellipsoid/area-length method. The volume defined by mitral annulus motion was 24 ml in normals, 16 ml in patients with cardiac failure and 48 ml in patients with mitral regurgitation while the ejection fraction was 51%, 19% and 53% respectively. Comparison between the volume of the truncuated cone and the ejection fraction in all 30 subjects revealed a statistically significant correlation (p less than 0.01). Thus, the bigger the volume determined by the mitral annulus motion during systole, the larger portion of the left ventricle is "atrialized", and a higher ejection fraction follows. Mitral annulus motion may provide new information about cardiac mechanics in normal and abnormal conditions.

Adolescent↗

PubMed1991

Effect of adrenergic blockade on pressure-related ventricular arrhythmias.

This paper examines whether adrenergic blockade (B1) may prevent the arrhythmogenic effect of acute arterial pressure (AP) elevation. In 7 anesthetized dogs iv propranolol (0.2 mg/kg) was given and in another 2 dogs stellate ganglion excision was performed. Before and after these B1 manoeuvres the AP was repeatedly increased by either elevating an open-air arterial pressure reservoir or administering iv metaraminol and decreased by abating the pressure reservoir. In a continuous recording of AP and ECG the systolic (S) AP and the presence (or absence) of ventricular arrhythmia (A) was noted. Before B1 A was noted in 652/1715 (38.0%) 5-sec periods at a SAP of 160.3 +/- 69.9 mm Hg which was significantly higher than in the 1063 5-sec periods without A (104.2 +/- 54.3) in all experiments. Following B1 it was impossible to cause A in 3 experiments. In the remaining experiments the A incidence was reduced (significantly in 5/9 experiments) to a total of 253/983 (25.7%) periods (P less than 0.001). In the 5/9 experiments with post-B1 A, the mean SAP was higher with (185.0 +/- 97.9 mm Hg) than without A (113.7 +/- 59.9 mm Hg) (significantly in 2/9 experiments). Following fitting of the SAP distributions before and after B1 to their common distribution (i.e. the same AP), the incidence of A was higher before than after B1 in all experiments (significantly in 7/9). It is concluded that B1 has an antiarrhythmic action on AP-related A. This antiarrhythmic effect seems to be due partly to an antihypertensive effect of B1 and partly to an antiarrhythmic effect of B1 for a given AP.

Adrenergic beta-Antagonists↗

PubMed1991

Induced electrophysiological isolation of the myocardium prevents ventricular fibrillation.

STUDY OBJECTIVE: to investigate whether an encircling procedure without ventriculotomy, not involving the endocardium, may have a protective effect against ventricular fibrillation (VF), by achieving a physiological rather than anatomic entrenchment. DESIGN: the occurrence of VF was tested by DC application within an area entrenched by a circular "dotted" line formed by LASER (Nd-Yag) point by point applications. The result was compared with that from similar DC applications before the successful LASER entrenchment or beyond the restricted area. SUBJECTS: 16 anaesthetized mongrel dogs, weights 14-20 kg were used. MEASUREMENTS AND RESULTS: VF occurred 13/118 times by applying DC within the entrenched area and 86/114 times by applying the current outside this area or before the intervention (P less than 0.0005). The pacing threshold was significantly (P less than 0.001) increased within the circumscribed area (4.625 +/- 5.335 vs 0.859 +/- 0.947 mA). The maximal rate at which the ventricles could be driven by pacing at double threshold intensity was not significantly altered by the encircling procedure. Histological examination showed crater-like epicardial destruction with necrosis, loss of myocardial striation, haemorrhage, and polymorphonuclear infiltration, extending about 0.5 cm from the necrotic tissue. The subendocardial area was spared showing only hyperaemia, while the endocardium was intact. CONCLUSIONS: Encircling a small area by LASER point by point applications prevents the occurrence of VF when DC is applied within the restricted area, while permitting the conduction of paced beats. The size of the encircled area necessary to this effect is of importance, possibly reflecting the critical mass needed for the occurrence and maintenance of VF.

Animals↗

PubMed1990

Pressure-related ventricular tachycardia.

A case with syncope on exertion and paced heart block is presented. Non-sustained ventricular tachycardia was seen on Holter monitoring and reproduced repeatedly by either exercise or an injection of an alpha agonist, but not with provocative electrophysiology. Antihypertensive treatment using a beta-blocker with endogenous sympathomimetic activity prevented recurrences. It is suggested that this is a case of pressure-related tachycardia.

Electrocardiography, Ambulatory↗