Transient Ventricular Fibrillation Research Articles

Elective Percutaneous Coronary Interventions (PCI) in 100 Cases in a Centre Without On-site Cardiac Surgery Support

Since its introduction in 1977, Percutaneous Coronary Interventions (PCI) is an important tool in the treatment of coronary artery disease (CAD). It is a retrospective analysis of data of 100 cases (132 vessels). The mean age was 50.9 years (range 30-70) with 90 (90%) male and 10 (10%) female. Indication of PCI includes acute and old MI, Chronic stable angina and unstable angina were 48 (48%), 33 (33%) and 19(19%) respectively. Procedure done in total 132 vessels among 100 patients. most of the cases were single vessels disease (SVD) {68 (68%} followed by double vessel disease (DVD) {30(30%)} , triple vessel disease (TVD) {02 (02%)} and chronic total occlusion (CTO) {02 (02%)}.Cobalt chromium was commonly used stent (117 (88.6%) followed by drug illuting stent (DES) 12 (9.1%) and bare metal stent (BMS) 3 (2.3%). Among the site of the stent insertion left anterior descending (LAD) 62 (47%), right coronary lesion (RCA) 37 (28), left circumplex artery (LCX) 33 (25%).Maximum stent length was 35 mm, minimum 10mm. Maximum stent diameter was 3.5 mm whereas minimum diameter 2.5 mm. The mean pretreatment reference diameter was 2.55 ± 0.20 mm and post treatment diameter 2.70 ± 0.45 mm. Angiographic, procedural and clinical success rate were 100%, 98% and 98% respectively. Major adverse cardiovascular event (MACE) {periprocedural MI} occurred in 2 (02 %) cases. Minor cardiovascular complications revealed vascular haematoma 2 (02%), bleeding from access site in 1 (01%), transient ventricular fibrillation (VF) in 3 (03%) cases. There was no hospital death, emergency CABG before discharge from hospital. Angiographic, procedural and clinical success rate were excellent with a little MACE and event free survival within 30 days follow up. So, PCI is a safe and effective method of myocardial revascularization irrespective of lesion morphology and type of stents used at immediate and 30 days follow up. DOI: http://dx.doi.org/10.3329/medtoday.v24i1.14106 Medicine TODAY Vol.24(1) 2012 pp.8-11

Prolongation of minimal action potential duration in sustained fibrillation decreases complexity by transient destabilization

Sustained ventricular fibrillation (VF) is maintained by multiple stable rotors. Destabilization of sustained VF could be beneficial by affecting VF complexity (defined by the number of rotors). However, underlying mechanisms affecting VF stability are poorly understood. Therefore, the aim of this study was to correlate changes in arrhythmia complexity with changes in specific electrophysiological parameters, allowing a search for novel factors and underlying mechanisms affecting stability of sustained VF. Neonatal rat ventricular cardiomyocyte monolayers and Langendorff-perfused adult rat hearts were exposed to increasing dosages of the gap junctional uncoupler 2-aminoethoxydiphenyl borate (2-APB) to induce arrhythmias. Ion channel blockers/openers were added to study effects on VF stability. Electrophysiological parameters were assessed by optical mapping and patch-clamp techniques. Arrhythmia complexity in cardiomyocyte cultures increased with increasing dosages of 2-APB (n > 38), leading to sustained VF: 0.0 ± 0.1 phase singularities/cm(2) in controls vs. 0.0 ± 0.1, 1.0 ± 0.9, 3.3 ± 3.2, 11.0 ± 10.1, and 54.3 ± 21.7 in 5, 10, 15, 20, and 25 µmol/L 2-APB, respectively. Arrhythmia complexity inversely correlated with wavelength. Lengthening of wavelength during fibrillation could only be induced by agents (BaCl(2)/BayK8644) increasing the action potential duration (APD) at maximal activation frequencies (minimal APD); 123 ± 32%/117 ± 24% of control. Minimal APD prolongation led to transient VF destabilization, shown by critical wavefront collision leading to rotor termination, followed by significant decreases in VF complexity and activation frequency (52%/37%). These key findings were reproduced ex vivo in rat hearts (n = 6 per group). These results show that stability of sustained fibrillation is regulated by minimal APD. Minimal APD prolongation leads to transient destabilization of fibrillation, ultimately decreasing VF complexity, thereby providing novel insights into anti-fibrillatory mechanisms.

Radiofrequency Energy Induced Ventricular Fibrillation in a Case of Idiopathic Premature Ventricular Contraction Originating from the Left Ventricular Papillary Muscle

A 15-year-old boy without structural heart disease was admitted for the treatment of frequent episodes of premature ventricular contractions (PVCs). Left ventricular mapping revealed that the origin of PVC was at the posterior papillary muscle. Diastolic small potentials were observed during sinus rhythm with a constant interval following QRS beats. This potential eventually coupled with the ventricular myocardium, resulting in the generation of PVC, and thus preceded QRS by 31 msec. Catheter ablation to this site induced non-sustained ventricular tachycardia, followed by transient ventricular fibrillation. Repeated application of radiofrequency energy eliminated PVC accompanied by the split of the diastolic potential.

Evidence that nonsustained polymorphic ventricular tachycardia causes syncope (data from implantable cardioverter defibrillators)

Patients with syncope account for ≅6% of hospital admissions and 3% of emergency room visits. 1 Kapoor W.N. Evaluation and management of syncope. JAMA. 1992; 268: 2553-2560 Crossref PubMed Scopus (245) Google Scholar Whether and how often nonsustained ventricular fibrillation (VF) or nonsustained polymorphic ventricular tachycardia (NSPMVT) can cause syncope is not entirely clear. In patients with the long QT syndrome, nonsustained Torsades de Pointes causing syncope is well described. Other reports, generally in patients with normal hearts, have occasionally described the association of NSPMVT and syncope. 2 Viskin S. Belhassen B. Idiopathic ventricular fibrillation. Am Heart J. 1990; 120: 661-671 Abstract Full Text PDF PubMed Scopus (188) Google Scholar , 3 Schwartz S.P. Studies on transient ventricular fibrillation. IV. Observations on clinical and graphic manifestations following revival of the heart from transient ventricular fibrillation. Am J Med Sci. 1936; 192: 808-815 Crossref Google Scholar , 4 Dubner S.J. Gimeno G.M. Elencwajg B. Leguizamon J. Tronge J.E. Quintero R. Ventricular fibrillation with spontaneous reversion on ambulatory electrocardiogram in the absence of heart disease. Am Heart J. 1983; 105: 691-693 Abstract Full Text PDF PubMed Scopus (33) Google Scholar , 5 Patt M.V. Podrid P.J. Friedman P.L. Lown B. Spontaneous reversion of ventricular fibrillation. Am Heart J. 1988; 115: 919-921 Abstract Full Text PDF PubMed Scopus (23) Google Scholar , 6 Masrani K. Cowley C. Bekheit S. El-Sherif N. Recurrent syncope for over a decade due to idiopathic ventricular fibrillation. Chest. 1994; 106: 1601-1603 Crossref PubMed Scopus (15) Google Scholar However, it is generally believed that VF is a sustained tachyarrhythmia that results in death 7 Olshansky B. Syncope overview and approach to management. in: Olshansky B. Syncope Mechanisms and Management. Futura Publishing Co, Inc, Armonk, NY1998: 15-71 Google Scholar and that NSPMVT is unusual as a cause of syncope. The current generation of implantable cardioverter defibrillators (ICDs) with intracardiac electrogram storage offer an opportunity to evaluate the incidence of NSPMVT relative to sustained VF and to document the association of syncope and presyncopal symptoms with these arrhythmias.

Results of the Jostent coronary stent graft implantation in various clinical settings: procedural and follow-up results.

The Jostent coronary stent graft (CSG) is composed of a PTFE layer sandwiched between two stainless steel stents, initially introduced for the treatment of coronary perforations and aneurysms with excellent results. By providing a mechanical barrier, this stent design also may be beneficial in the treatment of complex ulcerated lesions and in-stent restenosis by preventing debris protrusion and neointimal proliferation through the stent struts. To evaluate the safety and efficacy of this stent graft, we implanted 78 CSGs in 70 patients for a broad range of indications, including coronary perforations, aneurysms, degenerated saphenous vein grafts, complex lesions, and in-stent restenosis. The primary angiographic success rate (95.9%) was high, and using intravascular ultrasound (IVUS) guidance during stent implantation and high inflation pressures (19.3 +/- 3.2 atm), stent expansion with optimal symmetry was achieved in 94.7%. One limitation of the Jostent CSG was the side-branch occlusion rate (18.6%) and the resulting non-Q-wave infarction rate in seven cases (mean CK elevation, 238 U/l), acute Q-wave MI in two cases, and transient ventricular fibrillation in one patient after occlusion of the proximal RCA side branch without further complications. Subacute stent thrombosis occurred in four cases (5.7%) 7 to 70 days after stent implantation, despite using combined antiplatelet therapy with aspirin (ASA), ticlopidine, and/or clopidogrel for 30 days. Angiographic follow-up was available in 56 patients (80.0%) after a mean of 159 +/- 49 days, and follow-up IVUS was available in 38 cases. The overall restenosis rate (> 50% diameter stenosis) was 31.6% manifest primarily as edge restenosis (29.8% stent edge vs. 8.8% stent center; P < 0.001). IVUS examinations showed a minimal late lumen loss of 0.4 +/- 2.2 mm(2) within the center of the stent graft vs. 3.2 +/- 2.3 mm(2) at the stent edges (P < 0.001). The restenosis rate in the prespecified subgroups was 33.3% for saphenous vein grafts (2/6 lesions), 30.0% in complex lesions (6/20 lesions), and 38.5% (10/26 lesions) for the treatment of in-stent restenosis. Implantation of the Jostent CSG is feasible and safe, even in complex lesion subsets, and is associated with high primary success rates provided major side branches are avoided. The use of this stent may require an extended time course of antiplatelet therapy. Frequent focal stent edge renarrowing influences the overall restenosis rate. However, in treatment of complex in-stent restenosis and vein graft lesions, stent grafts may offer benefit over conventional therapies. Covered stents such as the JoMed coronary stent graft may become essential for bailout treatment of coronary perforations.

Hypertension‐Related Intermyocyte Junction Remodelling is Associated with a Higher Incidence of Low‐K+‐Induced Lethal Arrhythmias in Isolated Rat Heart

The aim of this study was to characterise the arrhythmogenic mechanisms involved in hypokalaemia-induced sustained ventricular fibrillation (SVF), in hypertensive rats. The hearts from rats with hypertension induced by the nitric oxide synthase inhibitor L-NAME, and age-matched normotensive controls, were perfused in Langendorff mode with oxygenated Krebs-Henseleit solution followed by a K(+)-deficient solution. In additional experiments, free intracellular Ca(2+) concentration ([Ca(2+)](i)) was measured using fura-2 in conjunction with an epicardial optical probe. The epicardial electrocardiogram was continuously monitored during all experiments. The gap junction protein connexin-43 and the ultrastructure of the cardiomyocytes were examined, and selected enzyme activities were measured in situ. There was a higher incidence of low-K(+)-induced SVF in the hearts of hypertensive compared to normotensive rats (83 % vs. 33 %, P < 0.05). Perfusion with a low-K(+)-containing solution lead to elevation of diastolic [Ca(2+)](i) that was accompanied by premature beats, bigeminy, ventricular tachycardia and transient ventricular fibrillation. These events occurred earlier with increased incidence and duration in the hearts of hypertensive rats (arrhythmia scores: hypertensive, 4.9 +/- 0.7; normotensive, 3.1 +/- 0.1; P < 0.05), which exhibited apparent remodelling accompanied by a significant decrease in the density of connexin-43-positive gap junctions. Moreover, low-K(+)-related myocardial changes, including local impairment of intermyocyte junctions, ultrastructural alterations due to Ca(2+) overload and intercellular uncoupling, and decreased enzyme activities were more pronounced and more dispersed in hypertensive than normotensive rats. In conclusion, nitric oxide-deficient hypertension is associated with decreased myocardial coupling at gap junctions. The further localised deterioration of junctional coupling, due to low-K(+)-induced Ca(2+) disturbances, as well as spatial heterogeneity of myocardial alterations including interstitial fibrosis, probably provide the mechanisms for re-entry and sustaining ventricular fibrillation.

Acute diabetes modulates response to ischemia in isolated rat heart.

Diabetic hearts are suggested to exhibit either increased or lower sensitivity to ischemia. Detrimental effects of prolonged ischemia can be attenuated by preconditioning, however, relatively little is known about its effects in the diseased myocardium. This study was designed to test the susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic heart. Rats were made diabetic with streptozotocin (45 mg/kg, i.v.). After 1 week, isolated Langendorff-perfused hearts were subjected to 30 min occlusion of LAD coronary artery without or with preceding preconditioning induced by one cycle of 5 min ischemia and 10 min reperfusion. Glycogen and lactate contents were estimated in the preconditioned and non-preconditioned hearts before and after ischemia. Diabetic hearts were more resistant to ischemia-induced arrhythmias: incidence of ventricular tachycardia (VT) decreased to 42% and only transient ventricular fibrillation (VF) occurred in 17% of the hearts as compared to the non-diabetic controls (VT 100% and VF 70% including sustained VF 36%; p < 0.05). Preconditioning effectively suppressed the incidence and severity of arrhythmias (VT 33%, VF 0%) in the normal hearts. However, this intervention did not confer any additional protection in the diabetic hearts. Despite higher glycogen content in the diabetic myocardium and greater glycogenolysis during ischemia, production of lactate in these hearts was significantly lower than in the controls. Preconditioning caused a substantial decrease in the accumulation of lactate in the normal hearts, whereby in the diabetic hearts, this intervention did not cause any further reduction in the level of lactate. In conclusion, diabetic rat hearts exhibit lower susceptibility to ischemic injury and show no additional response to preconditioning. Reduced production of glycolytic metabolites during ischemia can account for the enhanced resistance of diabetic hearts to ischemia as well as for the lack of further protection by preconditioning.

Is the Antiarrhythmic Effects of PA Related to Wavelength?

To the Editor: In their excellent article,1 Kwan et al found that (1) the antiarrhythmic effect of procainamide (PA) could not be attributed to the alteration in wavelength because it did not significantly affect wavelength during ventricular fibrillation (VF), and (2) the ability of PA to decrease the number of wavelets by preventing spontaneous wave breaks can represent a novel mechanism of antiarrhythmic drug action. Because PA antiarrhythmic and defibrillating effects in rats2 and guinea pigs3 cannot be explained by prolongation of wavelength, and the mechanisms of preventing wave break are not clear, let us discuss briefly the features required for antiarrhythmic defibrillating compounds. In an attempt to clarify the mechanisms underlying the maintenance of VF, we examined4 the factors involved in transient VF (TVF) versus sustained VF (SVF). No differences were found between cardiac muscle mass, heart rate, action potential duration, and effective refractory period of animals that exhibited TVF versus SVF. Similar …

Ventricular defibrillating properties of catecholamine uptake inhibitors

Ventricular fibrillation (VF) is a fatal event in humans unless electrical defribillation is applied within minutes. Recent publications describe spontaneous termination of VF in various animals and even in humans. Certain drugs can transfer a fatal, sustained VF (SVF) into a self-terminating, transient VF (TVF). Based on results obtained in animals of various species and ages, we have suggested that the occurrence of TVF requires a high cardiac catecholamine level at the time of VF. According to our hypothesis, drugs which decrease catecholamine reuptake by the sympathetic nerve terminals will increase the ability of the heart ventricles to defibrillate spontaneously. In the present study, we examined the effects of desipramine, maprotiline, mianserin, iprindole, cocaine and amphetamine on the type of VF in cats exhibiting SVF prior to the treatment. The results show that the ability of these compounds to transfer SVF to TVF is closely related to their potency to inhibit catecholamine reuptake. The establishment of the catecholamine related mechanisms of TVF may lead to the development of a new class of antiarrhythmic — defibrillatory drugs.

Hemi-front operation in surgery for single ventricle: A preliminary report

Mortality after Fontan operation is related to risk factors like ventricular hypertrophy, pulmonary artery deformity, and young age (infancy). Preliminary procedures may improve Fontan results. The hemi-Fontan operation includes atriopulmonary anastomosis and correction of all anatomical risk factors, but an atriopulmonary patch directs superior vena caval flow into both pulmonary arteries and inferior vena caval flow into the ventricle, thus maintaining cardiac output (modified Glenn physiology). We performed 17 hemi-Fontan procedures in 16 patients, 14 primarily (median age, 9 months) and 3 for takedown of a Fontan operation. The 14 primary operations were for hypoplastic left heart syndrome (5), pulmonary atresia with intact ventricular septum (4), and other (5). All patients had multiple risk factors. Extubation was at 18 hours (median), chest tube removal was at 3 days, and hospital discharge was at 8 days postoperatively. Important complications included subglottic stenosis, transient diaphragmatic paralysis, pulmonary artery stenosis and thrombosis requiring reoperation, and transient ventricular fibrillation. One patient required hemi-Fontan takedown, and this patient later (3 months postoperatively) became the only death. Fontan take-downs have had a high mortality rate. In 3 patients who tolerated Fontan operation poorly, converting Fontan to hemi-Fontan abruptly reversed the downhill course. For these patients, the operation was life-saving. Hemi-Fontan operation is safe and well-tolerated, even in infants, provides the advantages of modified Glenn physiology before Fontan operation, and may be especially useful for Fontan takedown after failed Fontan.

Ventricular self-defibrillation in mammals: age and drug dependence.

Ventricular fibrillation (VF) was electrically induced in cats, rabbits, guinea pigs and rats. In young animals of all species and also in old rats short transient VF (TVF) was followed by spontaneous reversion to normal sinus rhythm. Old cats, rabbits and guinea pigs had episodes of sustained VF (SVF) which did not terminate spontaneously; artificial electro-defibrillation was required. Dibenzepin converted the sustained response of old animals to a transient one. Verapamil antagonized the effect of dibenzepin in old animals and also changed the TVF in young animals to SVF. The effect of calcie age of the animal is an important factor in determining whether the fibrillatory red to an alteration in the properties of the cell membrane.

A case of transient ventricular fibrillation precipitated by psychogenic stress

A case of transient ventricular fibrillation precipitated by psychogenic stress

OPERATIVE HYPOTENSION FOR INTRACRANIAL VASCULAR SURGERY USING PACEMAKER-INDUCED VENTRICULAR TACHYCARDIA

✓ Temporary tachycardia of 130 to 160 beats/min was induced with a bipolar endocardial catheter pacemaker in 13 patients undergoing intracranial vascular surgery (nine for aneurysms, one for an arteriovenous anomaly, and three for brain tumors). It proved to be an effective method for achieving controlled hypotension of 25 to 40 mm Hg. Electrical pacing of the heart reduced diastolic filling time, lowered cardiac output, and produced systemic hypotension which was inversely proportional to the induced heart rate. Twelve patients made uneventful recoveries. One patient sustained intractable ventricular fibrillation while being paced at a rate of 180 to 190 beats/min and died. One patient developed transient ventricular fibrillation which was successfully converted. Cessation of pacing produced immediate return of systolic pressures to the prepacing levels. Although not without hazard, rapid ventricular pacing is recommended as an effective method for transiently lowering systemic blood flow during periods ...

Operative hypotension for intracranial vascular surgery using pacemaker-induced ventricular tachycardia.

✓ Temporary tachycardia of 130 to 160 beats/min was induced with a bipolar endocardial catheter pacemaker in 13 patients undergoing intracranial vascular surgery (nine for aneurysms, one for an arteriovenous anomaly, and three for brain tumors). It proved to be an effective method for achieving controlled hypotension of 25 to 40 mm Hg. Electrical pacing of the heart reduced diastolic filling time, lowered cardiac output, and produced systemic hypotension which was inversely proportional to the induced heart rate. Twelve patients made uneventful recoveries. One patient sustained intractable ventricular fibrillation while being paced at a rate of 180 to 190 beats/min and died. One patient developed transient ventricular fibrillation which was successfully converted. Cessation of pacing produced immediate return of systolic pressures to the prepacing levels. Although not without hazard, rapid ventricular pacing is recommended as an effective method for transiently lowering systemic blood flow during periods of potential or actual hemorrhage in intracranial vascular surgery.

Complete heart block with Stokes Adams attack from transient ventricular fibrillation.

A patient with complete heart block is described who developed a Stokes Adams attack due to transient ventricular tachycardia and fibrillation. The probable mechanism of the ventricular arrhythmia is discussed.

Electrocardiogram in ventricular rupture after myocardial infarction: Case report

The case of a 54-year-old white woman is presented in which an electrocardiogram was recorded at or shortly after the time of rupture of the left ventricle on the fifth day after a diaphragmatic myocardial infarction. The chief features of the terminal electrocardiogram were transient ventricular fibrillation, marked intraventricular conduction defect, rapidly decreasing amplitude of the QRS waves, development of first-degree atrioventricular block, intermittent cessation of ventricular (QRS) complexes, and finally, disappearance of atrial activity (cessation of P waves). Autopsy findings gave an excellent correlation with clinical and electrocardiographic findings. As far as can be determined, there has been no previous report of electrocardiographic findings at the time of ventricular rupture. Most of the changes described on the terminal electrocardiogram have been described before in the dying heart and are not diagnostic of myocardial rupture. However, the decreasing amplitude of the QRS complexes may have indicated developing hemopericardium secondary to ventricular rupture.

SUDDEN DEATH IN ACUTE MYOCARDIAL INFARCTION: REPORT OF A CASE, WITH OBSERVATIONS ON THE CAUSE, PREVENTION, AND MANAGEMENT

Excerpt Sudden death following acute myocardial infarction is a well recognized possibility. This unwelcome event, though more common in the first two weeks, may occur at any time after the onset o...

A Case of Adams-Stokes Attack Caused by Transient Ventricular Fibrillation in the Absence of Other Demonstrable Abnormality of the Heart

An unusual case of Adams-Stokes attack was reported. Several attacks of transient ventricular fibrillation were observed in a 13-year-old girl with apparently otherwise normal heart, during suspected influenzal infection. Procaine amide was dramatically effective in the present case.

Ventricular fibrillation during and after coronary artery occlusion: Incidence and protection afforded by various drugs ∗

The incidence of ventricular fibrillation during and after temporary experimental occlusion of the left anterior descending coronary artery or its branches was studied in 351 dogs. A standardized procedure of thirty-minute temporary occlusion of this artery was employed in 330. There is usually a critical period after twelve and up to fifteen minutes of ischemia which is characterized by a tendency to arrhythmia: extrasystoles, singly or in runs, ventricular tachycardia, or both extrasystoles and tachycardia if not a fatal ventricular fibrillation. Several instances of transient ventricular fibrillation were observed. Of 239 animals surviving thirty minutes of occlusion, 71 per cent developed ventricular fibrillation immediately after release of the artery, while only 28 per cent of 330 animals developed fibrillation during the occlusion. The re-establishment of blood flow to an area of the myocardium made ischemic for thirty minutes by occlusion of the anterior descending coronary artery is more likely to precipitate ventricular fibrillation than is the period of ischemia itself. Various drugs were evaluated in 324 dogs. Quinidine was the most effective drug in affording protection from ventricular arrhythmia during (7 per cent) and following (47 per cent) occlusion. Procaine, procaine amide and Apresoline offered good protection during the ischemic period. Apresoline and Regitine also reduced the incidence (44 and 37 per cent) of ventricular fibrillation upon reopening the ligature. Of the other drugs tested, only one, pendiomide, showed significant protection (52 per cent incidence). Systemic arterial pressures did not predict the onset of ventricular arrhythmia. Electrical countershock accomplished cardiac resuscitation in 75 per cent of the fibrillating dogs. From these experiments, quinidine appears to be the drug of choice in the prophylaxis of fatal ventricular arrhythmias.

Transient ventricular fibrillation: VI. Observations on the peripheral arterial pulse pressures in the course of transient ventricular fibrillation during established auriculoventricular dissociation

Transient ventricular fibrillation: VI. Observations on the peripheral arterial pulse pressures in the course of transient ventricular fibrillation during established auriculoventricular dissociation