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PubMed1987

In-hospital prognosis of patients with acute myocardial infarction complicated by primary ventricular fibrillation.

The in-hospital prognosis of patients with acute myocardial infarction complicated by primary ventricular fibrillation has not been satisfactorily defined. We addressed this question by studying patients with primary ventricular fibrillation derived from a large study (11,712 patients) of intravenous streptokinase in the treatment of acute myocardial infarction. Ventricular fibrillation was considered to be primary when it complicated a first myocardial infarction not associated with heart failure or shock and occurred within 48 hours of hospital admission. The 332 patients with primary ventricular fibrillation represented an overall incidence of 2.8 percent. A significant excess of in-hospital deaths was found in the patients with primary ventricular fibrillation as compared with those in the reference group (10.8 percent vs. 5.9 percent; relative risk, 1.94; 95 percent confidence interval, 1.35 to 2.78). Thrombolytic treatment with intravenous streptokinase did not afford protection against primary ventricular fibrillation. We observed that being over 65 years old had a protective effect against primary ventricular fibrillation (relative risk, 0.6; 95 percent confidence interval, 0.45 to 0.80). Our data do not indicate whether primary ventricular fibrillation is simply a marker for patients at increased risk of death or a direct cause of the increase in mortality. Our results do show, however, that primary ventricular fibrillation occurring in a coronary care unit is a negative predictor of short-term survival in patients with acute myocardial infarction.

Age Factors↗
PubMed1978

Left and right ventricular dimensions during ventricular fibrillation in the dog.

Ventricular dimensions by surface echocardiography and intraventricular pressures were monitored in 27 dogs before and during ventricular fibrillation (VF) induced by coronary embolization (nine dogs), potassium infusion (nine dogs) and calcium infusion (nine dogs). Left ventricular diameter (LVD) fell by an average of 10.3 mm during the first 30 s after the onset of VF induced by ischemia or potassium and remained smaller than the prefibrillation end-diastolic LVD during the ensuing 10 min. LVD fell during calcium infusion, and after the onset of VF it remained only slightly larger than the preinfusion end-systolic LVD. Right ventricular (RV) diameter increased progressively for the first 2 min during VF an average of 15.9 mm. The failure of LV size to increase during VF was explained by a pressure gradient inhibiting LV filling during the early phase of VF. Despite progressive RV filling, pressure in the more compliant RV remained lower than in the LV, which exhibited reduced compliance during VF. Therefore, cardiac dilation during VF appears to be confined to the RV, and inhibition to LV filling is an important feature of the syndrome.

Animals↗
PubMed1999

The circadian pattern of the development of ventricular fibrillation in patients with Brugada syndrome.

AIMS: Brugada syndrome is considered to be a distinctive subgroup of idiopathic ventricular fibrillation. Identification of the circadian pattern of ventricular fibrillation would contribute to the elucidation of its underlying pathophysiology, but this pattern remains unknown in patients with Brugada syndrome. METHODS: and Results A total of 12 consecutive Brugada syndrome patients (46+/-14 years, all male) who underwent implantation of an implantable cardioverter defibrillator were studied. The distribution of the time of ventricular fibrillation detection was examined and classified into four 6-hour time periods of the day. The mean follow-up period following implantation was 777+/-535 days. In six out of the 12 patients, ventricular fibrillation occurred during follow-up. The data logs revealed that ventricular fibrillation was detected 30 times (range, 3-9). Ventricular fibrillation was observed more frequently at night ( 1800 h to 0600 h) than in the day (0600 h to 1800 h) (93.3% [28/30] vs 6.7%[2/30], P<0.001), and during sleep than while awake (86.7% [26/30] vs 13.3%[4/30], P<0.001). Ventricular fibrillation occurred most frequently between midnight and 0600 h in patients with ventricular fibrillation episodes during sleep (76.9% [20/26] vs 23.1%[6/26], P<0.01). CONCLUSION: These results suggest that increased nocturnal vagal activity and withdrawal sympathetic activity may play an important role in the arrhythmogenesis of the Brugada syndrome.

Adult↗
PubMed1978

Ventricular fibrillation during cardiopulmonary bypass.

Changes in ultrastructure after induced ventricular fibrillation were studied in the normothermic and nonhypertrophic canine heart using a transmural myocardial biopsy method. Comparisons were made between subendocardial and subepicardial layers by the quantitative evaluation of ultrastructural changes in mitochondria and glycogen granules. Slight abnormalities characterized by interstitial edema, mitochondrial derangement, contraction bands, swelling of capillary endothelium were demonstrated throughout the myocardium following ventricular fibrillation. The myocardium following ventricular fibrillation did not demonstrate differences in ultrastructure between the subendocardial and subepicardial layers. These pathologic fine structural changes were at least in part reversible. Quantification of ultrastructure showed that mitochondria and glycogen granules were well preserved. It was suggested that the myocardium following ventricular fibrillation may be less affected by the no-reflow phenomenon after restoring normal coronary circulation.

Animals↗
PubMed1989

[Wolff-Parkinson-White syndrome and verapamil: apropos of a case of ventricular fibrillation].

Numerous highly effective antiarrhythmic agents are now available which have a powerful anti-arrhythmia action but may cause severe side effects in the case of inappropriate use. We report the case of a patient with WPW syndrome in whom inappropriate administration of verapamil during an episode of atrial fibrillation and rapid ventricular response caused ventricular fibrillation.

Adult↗
PubMed1995

Intermittent aortic crossclamping prevents cumulative adenosine triphosphate depletion, ventricular fibrillation, and dysfunction (stunning): is it preconditioning?

This study was designed to determine whether intermittent warm aortic crossclamping induces cumulative myocardial stunning or if the myocardium becomes preconditioned after the first episode of ischemia in canine models in vivo. The role of adenosine triphosphate catabolism and subsequent release of purines on reperfusion-mediated postischemic ventricular dysfunction and arrhythmias was assessed with the use of selective inhibitors of nucleoside transport, p-nitrobenzylthioinosine (NBMPR), and a specific adenosine deaminase inhibitor, erythro-9-[2-hydroxy-3-nonyl] adenine (EHNA). Thirty-two anesthetized dogs were instrumented to monitor left ventricular contractility, off bypass, by sonomicrometry. During cardiopulmonary bypass dogs were treated before ischemia with either saline solution (control group, n = 8) or EHNA (100 mumol/L) and NBMPR (25 mumol/L) (EHNA/NBMPR group, n = 8). Hearts were subjected to either 60 minutes of global ischemia and 120 minutes of reperfusion (n = 16) or 6 episodes of 10 minutes of global ischemia and 10 minutes of reperfusion, followed by 60 minutes of reperfusion (n = 16). Sixty minutes of sustained ischemia resulted in 80% loss of adenosine triphosphate and induced reperfusion-mediated ventricular fibrillation and severe left ventricular dysfunction in the control group. EHNA/NBMPR treatment augmented myocardial adenosine trapping during ischemia, attenuated ventricular fibrillation, and enhanced left ventricular functional recovery, despite similar depletion of adenosine triphosphate (80% loss). In the intermittent ischemia experiment, the first episode of 10 minutes of ischemia and reperfusion caused significant adenosine triphosphate depletion, ventricular fibrillation, and left ventricular stunning in both control and drug-treated groups. The prevalence of ventricular fibrillation was greater in the control group than in the drug-treated group after the first episode of ischemia (p < 0.05). Adenosine was the major nucleoside accumulated in the myocardium at the end of 10 minutes of ischemia in the EHNA/NBMPR-treated group (p < 0.05 versus control). Subsequent episodes of ischemia prevented ventricular fibrillation and did not cause cumulative left ventricular stunning in either group. Left ventricular function fully recovered in the EHNA/NBMPR-treated group after intermittent ischemia, but remained stunned in the control group. Unlike sustained ischemia, intermittent ischemia and reperfusion preserved myocardial adenosine triphosphate, limited purine release, and prevented ventricular fibrillation and cumulative stunning. These results suggest that intermittent ischemia and reperfusion augmented the endogenous protective mechanism or mechanisms of "preconditioning." Nucleoside trapping improved functional recovery after sustained or repetitive ischemia. It is concluded that adenosine triphosphate preservation or blockade of nucleoside transport may play an important role in the activation of endogenous myocardial protective mechanisms that "precondition" against subsequent ischemic stress.

Adenine↗
PubMed1995

Conversion of postischemic ventricular fibrillation with intraaortic infusion of potassium chloride.

BACKGROUND: Ventricular fibrillation after declamping of the aorta after cardioplegic arrest is commonly managed by direct-current countershock. However, in coronary artery bypass grafting, placement of the electrodes can cause mechanical damage to the grafts and anastomoses, and the surgical procedure must be interrupted. As an alternative, intraaortic infusion of potassium chloride through the arterial line from the heart-lung machine was investigated. METHODS: In a series of 100 patients with postischemic ventricular fibrillation (group P), 20 mmol of potassium chloride (plus 10 mmol later if necessary) was added to the oxygenator reservoir and perfused through the arterial line into the proximal aorta. The results were compared with those in a matched control group of 100 patients primarily treated with direct-current countershock (group DC). RESULTS: In group P, the ventricular fibrillation was effectively converted to a supraventricular rhythm in 82% of the patients. The remaining 18 patients required significantly (p < 0.005) fewer electric shocks than the patients in group DC. Serum K+ levels were slightly elevated for a short period after the potassium chloride infusion. Otherwise there were no significant differences in regard to incidence of heart block, temporary epicardial pacing, myocardial infarction, or atrial fibrillation between the two groups. CONCLUSIONS: Conversion of postischemic ventricular fibrillation with potassium chloride administered through the arterial line from the heart-lung machine is an effective, gentle, and convenient method. No side effects were noted.

Adult↗
PubMed2004

[Long survival with chronic ventricular fibrillation under support of uni-left-ventricular assist system].

Few minutes of suspended malignant ventricular arrhythmia may be permitted for the patient with left ventricular assist system (LVAS). However, longer and continuous ventricular arrhythmia, especially ventricular fibrillation (Vf), may induce the low output of LVAS, which leads circulatory collapse immediately. Our presenting case is a female dilated cardiomyopathy patient who has been supported with LVAS. Four months after the LVAS installation, her electrocardiogram has changed to Vf without any symptoms. Her ventricular function has never recovered, even ventricular tachycardia. She has been a candidate of heart transplantation for more than 19 months with this rare hemodynamic condition (LVAS+Vf), like the Fontan circulation. Her performance status is limited due to deceasing of the LVAS flow, which caused by the change of her position: 2.5-2.9 l/min (lie down) to 2.0 l/min (rise). Her peak VO2/W is 6.9 ml/min/kg measured by the cardio-pulmonary exercise test. However, she has developed her general status by doing rehabilitation program and is able to walk for more than 100-150 meters.

Adult↗
PubMed1982

A model of chronic ischemic arrhythmias: the relation between electrically inducible ventricular tachycardia, ventricular fibrillation threshold and myocardial infarct size.

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a "clinical" stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction. Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean +/- standard deviation 29 +/- 11 to 10 +/- 5 mA, p less than 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct. It is concluded that: (1) inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.

Animals↗
PubMed1975

Termination of ventricular fibrillation in dogs by depolarizing a critical amount of myocardium.

The role of a critical myocardial mass required to maintain ventricular fibrillation initiated by rapid ventricular pacing was studied by two methods in dogs placed on total cardiopulmonary bypass. In the first method, depolarization of a limited myocardial mass was accomplished by injecting potassium chloride into one or two coronary arteries. Injection of potassium chloride simultaneously into the left circumflex and left anterior descending coronary arteries abolished ventricular fibrillation more often than did injection into any other single or combination of two coronary arteries (P less than 0.0001). Ventricular fibrillation could not be reinitiated as long as the left ventricle remained inexcitable. Immersing the heart in a solution of potassium chloride or injecting the solution into the right and left ventricular cavities failed to terminate ventricular fibrillation. The second method evaluated the amount of current necessary to terminate ventricular electrodes, between two left ventricular electrodes and between one right ventricular and one left ventricular electrode. Electrical shocks of equal magnitude terminated ventricular fibrillation most often when those shocks were delivered between an electrode located at the right ventricular apex and an electrode located at the posterior base of the left ventricle, and least often when the shock was delivered between two right ventricular electrodes. Successful defribillation results when a critical amount of myocardium becomes depolarized by either potassium chloride or electrical discharge; depolarization of every cell in both ventricle is not necessary to terminate ventricular fibrillation in the entire heart.

Animals↗
PubMed1976

Experimental coronary occlusion in calves: the effect of hyperglycaemia on ventricular fibrillation threshold.

Measurements of ventricular fibrillation threshold (VFT) were made in two groups of bovine calves, each weighing 25 to 30 kg, before and after ligation of the anterior descending branch of the coronary artery. In the control group, the VFT was determined before occlusion of the anterior descending coronary artery, and the observations were repeated at 20-minute intervals after occlusion. A 33% reduction in VFT was observed 20 minutes after the occlusion. Prior loading with glucose by infusion of 100 ml of 10% glucose prevented the significant fall in VFT.

Animals↗
PubMed1976

Repetitive extrasystole as an index of vulnerability to ventricular fibrillation.

The assessment of ventricular vulnerability by inducing ventricular fibrillation (VF) presents limitations when neural activity is being investigated, especially in the unanesthetized animal. As repetitive extrasystoles (RE) have been observed to precede the occurrence of VF, it was relevant to determine whether the RE threshold provides a reliable index of cardiac susceptivility to fibrillation. The RE and VF threshold relationships were studied in 32 chloralose-anesthetized dogs during left stellate ganglion stimulation, vagus nerve stimulation, and beta-adrenergic blockage with practolol. The vulnerable period was scanned at 1-ms intervals and at 2-mA increments with a single, 2-ms, constant-current cathodal stimulus; RE and multiple RE were induced reproducibly when 66% and 82%, respectively, of the fibrillatory current was administered. The nadirs for RE and multiple RE were coincident in the cardiac cycle with the vulnerable-period threshold for VF. Stellate and vagal stimulation and beta-adrenergic blockade resulted in comparable changes in RE and VF thresholds and produced equivalent shifts in the cardiac cycle of the RE and VF vulnerable-period nadirs. These observations suggest that RE and VF phenomena share a common electrophysiologic basis and that the RE threshold can be used as an end point for measuring ventricular vulnerability to VF.

Animals↗
PubMed2005

Ventricular fibrillation frequency.

BACKGROUND: Ventricular-fibrillation (VF) wave frequency is known to decrease with prolonged, untreated VF. VF wave frequency is used as an algorithm to identify VF in AEDs and ICDs; yet the nature of the frequency change is not appreciated. METHODS: In this study, anesthetized pigs were used and VF was induced electrically. VF wave frequency was measured each second during VF for periods up to 200 sec. Defibrillation was achieved with transchest electrodes. VF wave frequency was plotted for each second during VF. In 2 animals, CPR was applied and VF wave frequency was measured. RESULTS: In all cases VF wave frequency decreased with increasing duration of VF. At the onset of VF, the VF wave frequency ranged from 5 to 12/sec. A plot of the normalized ratio of VF wave frequency during fibrillation to the VF frequency at induction decreased to between 0.1 and 0.8 of the initial frequency. In one of the animals, VF was initiated, CPR was provided and the VF wave frequency was measured over a 200-second period. Then, the procedure was repeated without CPR. Beyond 130 seconds, the VF frequency with CPR was higher than that without CPR, indicating myocardial oxygenation. CONCLUSION: Those who use VF wave frequency to identify the presence of VF should be aware of the nature of the VF wave frequency decrease with the passage of time.

Animals↗
PubMed1977

Influence of excitability on the ventricular fibrillation threshold in dogs.

The influence of the excitability threshold on the ventricular fibrillation threshold was studied in dogs during myocardial ischemia and potassium and aprindine infusion. Interventions that influenced excitability threshold were associated with similar changes in ventricular fibrillation threshold although the percent change in both values differed. Although it is possible that the interventions studied caused parallel but independent changes in excitability threshold and ventricular fibrillation threshold, it is likely that the excitability threshold influences the ventricular fibrillation threshold. An increase in excitability threshold could result in an increase in ventricular fibrillation threshold in spite of an increase in the actual tendency of the heart to fibrillate spontaneously. Such discordance between the "electrical stability of the heart" and the ventricular fibrillation threshold was found during myocardial ischemia.

Animals↗
PubMedDate not supplied

The effects of the d- and l-optical isomers of propranolol on the ventricular fibrillation threshold.

The minimum current required to induce ventricular fibrillation was determined in 22 sodium pentobarbital anesthetized open chest dogs in the presence of the d- or l-isomers of propranolol at concentrations of 0.2, 0.5, and 1.0 mg/kg. The hearts were paced from the right atrium at a constant basic cycle length of 350 msec and the current was delivered during the vulnerable period to the right ventricle as a 120 msec train of 4 msec square wave pulses at 100 Hz. The l-isomer of propranolol increased the ventricular fibrillation threshold (VFT) above control values at all concentrations; the maximum increase ranged from 17.8 to greater than 420.8% change from control. In contrast, the d-isomer caused only a small increase in the ventricular fibrillation threshold with the maximum increase ranging between 14.0 and 65.2% change from control. The maximum increase in VFT for the racemic mixture of propranolol was 44.7 to greater than 500.0% above control and was similar to the l-isomer alone. Since the beta-blocking potency of the l-isomer is 100 times the potency of the d-isomer we conclude that propranolol's action in increasing the ventricular fibrillation threshold is dependent on its beta-blocking effect.

Animals↗
PubMed1985

[Ventricular fibrillation in the initial phase of acute myocardial infarct].

In order to determinate the incidence, predictivity and prognosis of ventricular fibrillation in the early phase of acute myocardial infarction a series of 301 patients with acute myocardial infarction consecutively assisted by the Mobile Coronary Care Unit of Florence was analyzed. 151 patients (50.2%) received intensive care within 2 hours from the onset of the symptoms, 75 patients (24.9%) received intensive care between the second and sixth hour. 38 patients (12.6%) had at least one episode of ventricular fibrillation. 30% of the episodes of ventricular fibrillation happened within 1 hours from the onset of the symptoms, 47.4% within 2 hours, 74% within 6 hours. Serious arrhythmias complicated the early phase of acute myocardial infarction, but only sinus bradycardia seems to have a significant predicativity of ventricular fibrillation (P less than 0.05). We found that hospital survival resuscitated patients is strictly related to the time between early symptoms and the episode of ventricular fibrillation: 91% of the patients with ventricular fibrillation within 1 hour were discharged alive from hospital, 71% of those with ventricular fibrillation within 6 hours, 20% of those with ventricular fibrillation beyond 6 hours (P less than 0.01). The high rate and the favourable prognosis of ventricular fibrillation in the early phase of acute myocardial infarction must lead to a widespread implementation of rapid response emergency care systems away from hospital.

Humans↗
PubMed1997

Does in-hospital ventricular fibrillation affect prognosis after myocardial infarction?

AIM: The aim of this study was to estimate the prognostic information to be gained from ventricular fibrillation in patients with myocardial infarction. METHODS AND RESULTS: We studied 4259 consecutive patients with myocardial infarction admitted to one centre in 1977-1988. Five hundred and twenty-eight (12.4%) of the patients had ventricular fibrillation in hospital. The following risk factors were included in multivariate models to estimate their importance for 30-day and long-term (median 7 year) prognosis: age, gender, ventricular fibrillation, congestive heart failure, pulmonary oedema, cardiogenic shock, other cardiac arrest and atrial fibrillation. We found that the odds ratio for death on days 6.30 was 6.34 (3.55-11.30, 95% confidence limits, P < 0.001) for patients with primary ventricular fibrillation (without heart failure) and 4.06 (2.68-6.14, P < 0.001) for patients with ventricular fibrillation secondary to heart failure compared to patients without ventricular fibrillation. For patients surviving more than 30 days, relative risk of death in those with ventricular fibrillation was 1.11 (95% confidence interval 0.93-1.34, P = 0.26). Logistic regression analysis of relative risk associated with ventricular fibrillation in time intervals, indicated that the importance of ventricular fibrillation for risk of death was exhausted during the initial 60 days after infarction. CONCLUSION: Ventricular fibrillation is associated with an independent increased risk of death within 0-60 days after infarction. After this period, the prognosis in survivors of ventricular fibrillation does not differ significantly from patients without ventricular fibrillation.

Adult↗