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PubMed2003

Aldosterone receptor blockade improves left ventricular remodeling and increases ventricular fibrillation threshold in experimental heart failure.

OBJECTIVES: To investigate the effects of aldosterone receptor blockade in postinfarction heart failure. METHODS: Eighty-seven rats with moderate myocardial infarction were randomized to receive either no drug or canrenone, the active metabolite of spironolactone, 20 mg/kg/day, or ramipril, 1 mg/kg/day, or a combination of the two drugs. Treatment was initiated 1 month after coronary ligation and lasted 4 weeks. Echocardiography was performed at baseline and after 4 weeks. LV catheterization, isolated heart studies, morphometric histology, myocardial norepinephrine and SERCA-2 mRNA were assessed at the end of the treatment period. RESULTS: Infarct sizes were 33+/-3, 32+/-3, 34+/-3, and 34+/-4% in the placebo, canrenone, ramipril, and combination groups, respectively. Canrenone attenuated LV remodeling, improved LV systolic and diastolic function, and markedly reduced interstitial and perivascular fibrosis. These effects were increased by concomitant ramipril therapy. Moreover, myocardial norepinephrine content was decreased while ventricular fibrillation threshold significantly augmented by canrenone. SERCA-2 levels remained unchanged. CONCLUSIONS: Canrenone attenuated LV dilation and interstitial remodeling, and improved LV filling dynamics and systolic function in the rat model of postinfarction heart failure. Addition of ramipril conferred further cardioprotection. Canrenone also reduced myocardial norepinephrine content and increased ventricular fibrillation threshold. The data provide a potential explanation for the decreased sudden death observed in the RALES study. The mechanisms of action of aldosterone inhibition are still poorly understood, despite its proven efficacy in heart failure. Rats with postinfarction heart failure were randomized to receive for 1 month either no drug or canrenone, or ramipril, or a combination of canrenone and ramipril. Canrenone treatment was associated with a significant attenuation of LV dilation, better LV diastolic and systolic dynamics, and a marked reduction of reactive fibrosis. These effects were enhanced by concomitant ramipril therapy. Moreover, canrenone increased ventricular fibrillation threshold and reduced myocardial norepinephrine content. The data may explain the reduced mortality demonstrated by the RALES.

Animals↗

PubMed2000

Electrophysiological deterioration during long-duration ventricular fibrillation.

BACKGROUND: Probability of survival from sudden cardiac arrest caused by ventricular fibrillation (VF) decreases rapidly with fibrillation duration. We hypothesized that cellular ischemia/fibrillation-induced electrophysiological deterioration underlies decreased survival. METHODS AND RESULTS: We determined fibrillation monophasic action potential (MAP) morphology including action potential frequency content, duration, cycle length, developing diastolic intervals, and amplitude as a function of ischemic fibrillation duration in 10 isolated rabbit hearts. We also correlated ECG frequency (used clinically) and MAP amplitude and frequency. Fibrillation cycle length and diastole duration increased, whereas APD(100) shortened significantly with time (P:<0.001). Between 1 and 3 minutes, diastole appeared primarily as the result of APD(100) shortening, with only small changes in cycle length. Between 2 and 5 minutes, diastole increased primarily as the result of increased cycle length. Diastole developed progressively from 5% of VF cycles at 5 seconds to approximately 100% of VF cycles by 120 seconds (P:<0.001). Diastole increased from 1% of cycle length at 5 seconds to 62% at 5 minutes. Its duration increased from 4.7 ms at 5 seconds to 90 ms at 5 minutes (P:<0.001). Both MAP and ECG 1/frequency closely correlated with fibrillation cycle length. CONCLUSIONS: These results show a rapid and progressive electrophysiological deterioration during fibrillation, leading to electrical diastole between fibrillation action potentials. This rapid deterioration may explain the decreased probability of successful resuscitation after prolonged fibrillation. Therefore, a greater understanding of cellular deterioration during fibrillation may lead to improved resuscitation methods, including development of specific defibrillator waveforms for out-of-hospital cardiac arrest.

Action Potentials↗

PubMed2002

Action potential duration restitution and ventricular fibrillation due to rapid focal excitation.

The focal source hypothesis of ventricular fibrillation (VF) posits that rapid activation from a focal source, rather than action potential duration (APD) restitution properties, is responsible for the maintenance of VF. We injected aconitine (100 microg) into normal isolated perfused swine right ventricles (RVs) stained with 4-[beta-[2-(di-n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) for optical mapping studies. Within 97 +/- 163 s, aconitine induced ventricular tachycardia (VT) with a mean cycle length 268 +/- 37 ms, which accelerated before converting to VF. Drugs that flatten the APD restitution slope, including diacetyl monoxime (10-20 mM, n = 6), bretylium (10-20 microg/ml, n = 3), and verapamil (2-4 microg/ml, n = 3), reversibly converted VF to VT in all cases. In two RVs, VF persisted despite of the excision of the aconitine site. Simulations in two-dimensional cardiac tissue showed that once VF was initiated, it remained sustained even after the "aconitine" site was eliminated. In this model of focal source VF, the VT-to-VF transition occurred due to a wave break outside the aconitine site, and drugs that flattened the APD restitution slope converted VF to VT despite continuous activation from aconitine site.

Aconitine↗

PubMed1979

[pH changes and the K+ and Na+ concentration in the blood of the coronary vein in experimental myocardial infarct complicated and not complicated by ventricular fibrillation].

It was found that following occlusion of the coronary artery in dogs, the rate of increase in K+ concentration in blood plasma draining directly from the focus of ischemia is greater in cases complicated by ventricular fibrillation. Fibrillation always occurs against the background of a decrease in pH and an increase in the K+ level in blood plasma draining from the focus of ischemia. It is suggested that inhibition of the development of disorders of acid-base and ion equilibrium in the myocardium would be an effective means of preventing ventricular fibrillation in the acute stage of myocardial infarction.

Acid-Base Imbalance↗

PubMed1984

Aclarubicin-associated QTc prolongation and ventricular fibrillation.

A marked prolongation of QTc (corrected QT interval for heart rate) in ECG developed in two patients with acute leukemia during induction chemotherapy with aclarubicin, one of the anthracycline antibiotics. This ECG change was followed by ventricular fibrillation. No signs or symptoms of congestive heart failure were noted. The outcome in one case was fatal; in the other case, the ECG change was reversible. These observations suggest that QTc prolongation, which has been considered to be a sign of acute cardiotoxicity of anthracycline derivatives, may signal a clinical risk of ventricular fibrillation.

Aclarubicin↗

PubMed2006

Vagal nerve-mediated vasospasm-induced lethal ventricular fibrillation.

We report a case of variant angina complicated by lethal ventricular fibrillation. Serial ambulatory electrocardiogram monitoring revealed high-frequency spectra reflecting augmented vagal nerve activity preceding the vasospastic episodes. Our case suggests that heart rate variability analysis can help identify potential unexpected sudden cardiac death in patients with variant angina.

Angina Pectoris↗

PubMed1987

Refractory symptomatic ventricular tachycardia and ventricular fibrillation in elderly patients.

The problem of refractory life-threatening ventricular tachyarrhythmias in elderly patients has not been previously studied. To determine if clinical, anatomic, or electrophysiologic variables and prognosis are significantly different in elderly subjects, 49 elderly (68 to 84 years) and 44 younger (44 to 53 years) survivors of refractory symptomatic ventricular tachycardia and/or ventricular fibrillation secondary to coronary artery disease were studied. Elderly patients displayed more extensive anatomic coronary artery disease, with 80 percent having three-vessel disease in comparison with 30 percent of the younger patients (p less than 0.001). Prior myocardial infarction, heart failure, and cardiomegaly were more common in the elderly group (p less than 0.01, p less than 0.001, and p less than 0.034, respectively), whereas angina was more common in the younger group (p less than 0.001). In 55 percent of the elderly patients and 58 percent of the younger patients, electrophysiologic testing demonstrated inducible sustained ventricular tachycardia that required treatment with an investigative antiarrhythmic drug and/or cardiac surgery, including implantation of an automatic defibrillator. Elderly patients tolerated aggressive evaluation as well as did younger patients, and despite the difference in clinical and anatomic findings, long-term survival curves were similar, although the probability of survival at 20 months was 62 percent in the elderly and 80 percent in the younger patients. This difference in early survival is explained by eight surgical deaths in the elderly group, compared with two in the younger group.

Age Factors↗

PubMed1976

Cyclic adenosine monophosphate, ventricular fibrillation, and antiarrhythmic drugs.

It is proposed that the development of ventricular fibrillation in the context of ischaemic heart-disease and myocardial infarction can be related to accumulation of cyclic adenosine 3',5' monophosphate (A.M.P.) in the ischaemic zone. The known electrophysiological and metabolic actions of cyclic A.M.P. are consonant with the hypothesis, which also provides a framework for the better understanding of the action of antiarrhythmic drugs.

Adrenergic beta-Antagonists↗

PubMed2000

Left ventricular myocardial adenosine triphosphate changes during reperfusion of ventricular fibrillation: the influence of flow and epinephrine.

OBJECTIVE: To determine whether epinephrine in combination with high flow worsens left ventricular (LV) myocardial high-energy phosphate stores during reperfusion of ischemic ventricular fibrillation (VF). DESIGN: Blinded, prospective block randomized, placebo controlled study. SETTING: University medical center research laboratory. SUBJECTS: A total of 22 mixed breed swine weighing 22.0+/-3.3 kg (SD). INTERVENTIONS: Open-chest swine, anesthetized with alpha-chloralose, underwent 10 mins of nonperfused VF followed by reperfusion with cardiopulmonary bypass for 90 mins and then defibrillation. Animals were block randomized to four groups for reperfusion: Group 1 (n = 5), high flow (100 mL/kg/min) and epinephrine (2.5 microg/kg/min); Group 2 (n = 5), high flow and placebo; Group 3 (n = 6), low flow (30 mL/kg/min) and epinephrine; and Group 4 (n = 6), low flow and placebo. MEASUREMENTS AND MAIN RESULTS: In vivo LV creatine phosphate (CP) and adenosine triphosphate (ATP) were determined using whole wall and spatially localized 31P NMR spectroscopy at 4.7 Tesla. During perfusion of the fibrillating myocardium, epinephrine significantly increased aortic pressure (p < .05) and improved defibrillation rates (p < .01). ATP levels during reperfusion were significantly decreased within all groups compared with baseline. There were no differences in ATP levels between groups. High flow, independent of epinephrine, was associated with increased preservation of ATP (p < .05), increased CP/ATP ratios (p < .02) in all layers of the LV wall, and decreased aortic and cardiac vein lactates (p < .001). CONCLUSIONS: Epinephrine, in combination with flow higher than standard cardiopulmonary resuscitation flows, increased perfusion pressure and defibrillation rates, but did not significantly alter myocardial ATP during VF reperfusion in the in vivo heart Reperfusion flow, independent of epinephrine, is a critical determinant of myocardial ATP preservation.

Adenosine Triphosphate↗

PubMed1975

[Histoxic hypoxia as one of the causes of ventricular fibrillation and decreased myocardial contractility].

Long-lasting infusions of adrenalin were demonstrated to result in histotoxic hypoxy of the myocardium and its decreased contractility. After a preliminary ligation of several branches of the coronary arteries such situations often caused ventricular fibrillation. The restoration of the myocardial contractility and of the oxydation processes was achieved by the administration of Unithiol, Methionin, Cystein and Succimere. The latter often produce an unusual effect--arrest of ventricular fibrillation and restoration of a normal cardiac rhythm without electric defibrillation. The beneficial effect of these drugs is attributed by the authors to the presence of thiol groups in their structure.

Animals↗

PubMed2000

Electrophysiological instability in the acute phase: prognostic significance of early ventricular fibrillation in acute myocardial infarction.

BACKGROUND: In the prognostic stratification of patients affected by AMI is important to evaluate, besides the assessment of left ventricular function and residual ischemia, the presence of electrophysiological instability. METHODS: We have analysed 15 patients all affected by AMI complicated by early ventricular fibrillation. During the hospital phase we evaluated the E.F.% (ECHO) and the presence of late ventricular potentials (SAECG). After hospital discharge we followed up the patients for 6 months. RESULTS: None of the patients died during the hospital phase while the posthospital cardiac mortality was 20%. The three patients dead during the follow-up had an AMI localized in the anterolateral wall of the left ventricle, an E.F.% less than 40% and LVP positive in the hospital phase. Besides the clinical course was complicated by cardiac failure. CONCLUSIONS: We conclude that these three patients are a "high risk profile subgroup" and should be submitted to extensive evaluation with cardiac catheterization, coronary arteriography and programmed ventricular stimulation.

Adult↗

PubMed1983

The repetitive ventricular response: relationship to ventricular fibrillation threshold in dogs.

The experiments investigated the hypothesis that the occurrence of repetitive ventricular responses elicited by the ventricular extrasystole (VES) technique are an indicator of ventricular vulnerability to fibrillation. A comparison was made between the incidence of repetitive responses elicited by the VES technique and the minimum electrical energy (VFT technique) necessary to elicit repetitive responses and ventricular fibrillation in normal dogs, dogs with acute infarction, and dogs with chronic infarction. The VES technique produced repetitive responses in 14 of 46 sites. Responses were of at least three types: (1) bundle branch re-entry; (2) activation at the pacing site, and (3) activation at the infarct zone. In contrast repetitive responses and the onset of fibrillation produced by the VFT technique appeared to be a single type with earliest activation at the pacing site. There were no differences in the ventricular fibrillation thresholds between dogs with and without repetitive responses produced by the VES technique. Thus the incidence of VES technique-induced repetitive responses is not a reasonable predictor of ventricular vulnerability to fibrillation. However, in 2 dogs with lower ventricular fibrillation thresholds, repetitive responses originating at the infarct zone were induced by the VES technique. Occurrence of these repetitive responses may be indicative of ventricular vulnerability to fibrillation.

Animals↗

PubMed1975

Ventricular fibrillation threshold and vulnerable period in the isolated perfused rat heart.

Ventricular fibrillation threshold (VFT) measurements were obtained in the isolated perfused rat heart. Detailed morphology of the vulnerable period (VP) could be described by stimulating repeatedly at increasing levels of stimulus energy. Addition of lignocaine to the system caused an elevation of VGT, but also led to a delay of the VP to the end of the QT interval. The implications of these findings for the understanding of VFT measurements are discussed.

Animals↗

PubMed1995

[Characteristics of body surface mapping in the cases of idiopathic ventricular fibrillation].

Body surface mapping was recorded in three patients with idiopathic ventricular fibrillation (VF). A late r' wave appeared and disappeared in the precordial leads in all three patients. In one case, the late r' wave appeared with epithides of VF. In the presence of the late r' wave, the QRS duration was extremely prolonged. However, the appearance time of the breakthrough in the QRS isopotential map was not significantly prolonged. The time of the peaks of the r' wave was elongated in the mid anterior chest. These findings suggest that peripheral conduction disturbances in the right ventricle are related to the occurrence of VF in patients with idiopathic VF.

Adult↗

PubMedDate not supplied

The changing incidence of ventricular fibrillation in Milwaukee, Wisconsin (1992-2002).

OBJECTIVES: To investigate the changes in annual incidence and survival of out-of-hospital cardiac-etiology arrests of different initial rhythms, particularly ventricular fibrillation (VF) and ventricular tachycardia (VT), among adults (> 21 years old) in Milwaukee County between 1992 and 2002 and establish correlations with patient and emergency medical services (EMS) system-dependent factors. METHODS: The study was a retrospective, observational study of all adult (> 21-year-old) patients with out-of-hospital cardiac-etiology arrests with identifiable rhythm and resuscitation attempted by the Milwaukee County EMS system from 1992 to 2002. Nine thousand one hundred seventy cases were enrolled. Primary outcome measures were changes in annual incidence of initial cardiac arrest rhythm, with a focus on VF/VT. Secondary outcome measures were changes in survival to hospital admission and hospital discharge for VF and VT. Patient and EMS system factors potentially affecting the outcome measures were identified and modeled using multivariate logistic regression. RESULTS: The incidence of out-of-hospital VF/VT arrests decreased steadily from 37.1 per 100,000 in 1992 to 19.4 per 100,000 in 2002. While the incidences of pulseless electrical activity and overall cardiac arrest remained unchanged, the incidence of asystole during the study period increased from 27.3/100,000 to 44.9/100,000. Multivariate regression analyses revealed that age < 80 years, male gender, white race, previous cardiac surgery, and cardiac history were patient-dependent factors predictive of VF/VT. Witnessed arrest, public location, and shorter response time were EMS system-dependent factors predictive of VF/VT. Based on observed trends, none of these correlated factors could explain the decrease in the incidence of VF/VT arrests. Rates of patient survival to hospital admission and discharge were not significantly changed over time. EMS system factors predictive of survival to admission and discharge were witnessed arrest, public location, and decreased number of defibrillations. Prior cardiac surgery and absence of chronic problems were the only patient factors predictive of survival to hospital admission but were not significantly related to survival to hospital discharge. CONCLUSIONS: The incidence of out-of-hospital cardiac arrests in adult patients with presenting rhythm of VF/VT declined, while an increase in asystole occurred. This was not explained by any patient or EMS system-dependent factor. Rate of survival for VF/VT arrest did not significantly change over time. Survival was primarily influenced by EMS system factors and unrelated to patient-dependent factors.

Adult↗

PubMed2005

[Resuscitation in ventricular fibrillation: what is essential?].

Prognosis of prehospital cardiac arrest due to ventricular fibrillation is dependent on the first minutes, as survival decreases by 10% for each minute by which resuscitation attempts are delayed. Thus, early defibrillation plays a key role in improving outcome of cardiac arrest victims. The effectiveness of automated external defibrillators (AEDs) in this setting has been proven by several clinical trials. There remains controversy with regard to using AEDs in the in-hospital setting, as well as the approach of "public access" defibrillation. Whereas the use of intravenous antiarrhythmic drugs, particularly amiodarone, remains controversial, new data support the use of vasopressine instead of epinephrine as vasopressor drug in cardiac arrest patients. The present review aims to focus on the above mentioned aspects as well as on the changes to the present ILCOR guidelines which have led to modification of the resuscitation guidelines of the European Resuscitation Council (ERC).

Anti-Arrhythmia Agents↗

PubMed1991

[Prevention and treatment of isoproterenol induced ventricular fibrillation in rats by aqueous extract of Salvia miltiorrhiza].

Acute fatal ventricular fibrillation (VF) in male Sprague-Dawley rats was induced by subcutaneous injection of isoproterenol (1 mg or 5 mg/kg body weight) to two groups of rats of different body weights (525 +/- 21 g or 387 +/- 11 g) respectively. VF occurred in all control rats resulting in 96% death with only 4% spontaneously reverted and survived. Pretreatment of animals, with or without pentobarbital anaesthesia, with an aqueous extract of Salvia miltiorrhiza (SM-H, i.p., 5 g herb/kg body weight) significantly reduced J-point displacement and VF induced by isoproterenol. Survival rate was significantly raised compared with the control (P less than 0.05). Immediate intravenous injection of SM-H (5 g herb/kg body weight) to poisoned rats which developed VF caused 71% of them to recover temporarily their sinus rhythm and significantly prolonged their survival time (P less than 0.05).

Animals↗

PubMed1988

Paradoxical increase of ventricular fibrillation threshold in response to coronary sinus obstruction.

We determined the ventricular fibrillation threshold (VFT) changes in response to graded coronary sinus (CS) obstruction in 13 chloralose-anesthetized dogs with fixed heart rate (150 min-1, mean systemic arterial pressure (80 mm Hg), and cardiac index (100 ml/min.kg-1 body weight). VFT in milliamperes (VFTmA) increased linearily with CS pressure (CSP) increases up to 41.2 +/- 1.4 mm Hg (VFTmA = 6.5 + 0.14 CSP mm Hg, p less than 0.01). Total coronary venous effluent (CBF) did not change significantly, suggesting compensatory coronary vasodilation. Myocardial O2 consumption also remained unchanged. At higher CSP, both CBF and VFT declined precipitously (VFTmA = 20.9 - 0.27 CSP mm Hg, p less than 0.02). With simultaneous increases of systemic arterial along with CSP, VFT increased again along with the CSP-induced reduction of gradient until it reached 42.8 +/- 3.2 mm Hg. We conclude that with coronary venous obstruction, despite coronary perfusion gradient reduction to about 40 mm Hg, CBF remains constant. This constant flow vasodilation is associated with substantial (82%) VFT increase. The mechanism may involve enhanced homogeneity of CBF distribution and increased extracellular fluid.

Animals↗