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[Change in the opioid peptide level in the heart and blood plasma during acute myocardia ischemia complicated by ventricular fibrillation].

After occlusion of the anterior descending coronary artery content of opioid peptides was increased 2-3-fold in blood plasma of all the rats with and without ventricular fibrillation. Content of Leu-enkephalin was decreased in ischemic and non-ischemic regions of myocardium under conditions of ventricular fibrillation. At the same time, concentration of Met-enkephalin in myocardium was increased in the acute ischemia independently on the effect of fibrillation. Synthetic enzyme-resistant derivative of Leu-enkephalin, administered before acute myocardial ischemia, prevented a decrease in the ventricular fibrillation threshold caused by the occlusion. Alteration of the Leu-enkephalin content in heart tissue appears to be importance in pathogenesis of ventricular fibrillation developed after acute myocardial ischemia.

Acute Disease↗

Pharmacological analysis of established ventricular fibrillation.

1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.

Animals↗

Reducing the risk of ventricular fibrillation by adding sodium to ionic and non-ionic contrast media with low iodine concentration. Coronary perfusion of the isolated rabbit heart with meglumine diatrizoate or iopentol at 140 mg I/ml and 0-154 mmol Na+/l.

To compare the fibrillatory propensity of low concentrations of contrast media (140 mg I/ml) the ionic, ratio 1.5, contrast medium meglumine diatrizoate, the non-ionic, ratio 3, medium iopentol and equimolar glucose (0.37 mol/l) were perfused into 35 isolated rabbit hearts. The three substances were compared at three levels of sodium concentration (0.77 and 154 mmol Na+/l). Meglumine diatrizoate without sodium caused the highest frequency of ventricular fibrillation (91%). Iopentol without sodium caused a significantly lower frequency of ventricular fibrillation (17%). Glucose without sodium caused no fibrillation. The addition of 77 or 154 mmol Na+/l significantly decreased the frequency of ventricular fibrillation of both meglumine diatrizoate (3% and 6%) and iopentol (0%). Meglumine diatrizoate with sodium added caused a lower frequency of ventricular fibrillation than iopentol without sodium. At equal sodium concentrations (0.77 and 154 mmol Na+/l) glucose caused smaller reduction in contractile force and heart rate than iopentol, and iopentol caused smaller reduction in contractile force and heart rate than diatrizoate. It is concluded that addition of sodium to ionic or non-ionic contrast media without sodium decreases the risk of ventricular fibrillation.

Angiocardiography↗

Left ventricular function after repeated episodes of ventricular fibrillation and defibrillation assessed by transoesophageal echocardiography.

BACKGROUND: Investigators studying the effects of cardioverter-defibrillators on left ventricular systolic function have given only minor attention to the diastolic effects. OBJECTIVES: The purpose of this study was to investigate the impact of repeated episodes of ventricular fibrillation and defibrillation on systolic function and diastolic filling of the left ventricle during non-thoracotomy implantation of a cardioverter-defibrillator. METHODS: Systolic function and diastolic filling of the left ventricle were assessed peri-operatively on a beat-by-beat basis using a transoesophageal echo-Doppler technique in 12 patients during > or = 4 episodes of ventricular fibrillation and defibrillation. Systolic function was assessed from the fractional area change and diastolic filling from the E/A ratio. Arterial blood pressure and the ECG were recorded continuously. RESULTS: Blood pressure and heart rate did not change significantly throughout the procedure. The systolic function, similarly, was not significantly affected; the only changes were seen in the first two beats after defibrillation when the mean fractional area increased from 0.2 +/- 0.01 to 0.4 +/- 0.02 and 0.3 +/- 0.02, respectively (P < 0.001). Diastolic filling was, however, impaired as reflected by a decrease in the E/A ratio from 2.6 +/- 0.5 before to 1.6 +/- 0.4 (P < 0.01) after repeated threshold tests. CONCLUSIONS: While the combined ischaemic and electrical trauma caused by repeated episodes of ventricular fibrillation and defibrillation during the implantation of a cardioverter-defibrillator did not cause any systolic dysfunction, diastolic filling was significantly impaired.

Adult↗

Energy doses for treatment of out-of-hospital pediatric ventricular fibrillation.

AIM: To investigate the energy dose used to treat out-of-hospital pediatric ventricular fibrillation and the survival rates of these patients. METHODS: We reviewed three emergency medical systems (EMS) for their reports of patients under 1 month to 18 years who received shocks for ventricular fibrillation to determine the energy of each shock as well as other patient and care characteristics. Each patient's weight was estimated at the age-appropriate 50th and 95th percentiles. Patients were then grouped as receiving recommended energy doses (2 to < or = 4 J/kg), moderately high energy doses (> 4-6 J/kg), and high energy doses (> 6 J/kg). RESULTS: Of 57 patients identified, 54% were male, with a mean age of 11 years, range 2 months to 17 years. Ventricular fibrillation was the initial rhythm in 80% (43/54) of patients. The mean number of shocks delivered was 3, with < or = 2 shocks delivered to 28 (49%) and > or = 5 shocks delivered to 10 (18%) patients. When evaluating all 185 shocks using the 50th percentile estimated weight, 45 (24%) shocks were at recommended doses, 56 (30%) were at moderately high energy doses, and 84 (45%) were high energy doses. Elevated energy dose was associated with an increasing number of shocks and lack of bystander CPR (p < .05). Nineteen (33%) patients survived to hospital discharge having received total doses up to 73 J/kg. Energy dose was not related to survival. CONCLUSION: In this observational, multicenter out of hospital experience, children received a wide range of defibrillation doses, often exceeding recommended doses and equivalent to adult energy levels. Survival occurred at low and very high energy doses.

Adolescent↗

[Level of enkephalins and cyclic nucleotides in the myocardium in ventricular fibrillation caused by experimental myocardial infarct].

Ventricular fibrillation, caused by the occlusion of the anterior descending coronary artery, results in leu-enkephalin level decrease in ischemic and non-ischemic zones of myocardium. The fibrillation is found to induce cAMP increase in the ischemic zone and cGMP increase in the normal circulation zone. cGMP and leu-enkephalin level correlates with fibrillation duration. Enkephalins and cyclic nucleotides are suggestive of being of importance in heart rythm disturbances pathogenesis.

Animals↗

[Clinical characteristics of ventricular tachycardia and ventricular fibrillation in exercise stress testing].

OBJECTIVES: Ventricular tachycardia (VT) and ventricular fibrillation (Vf) induced in exercise stress testing should be treated urgently, although the occurrence of arrhythmia is rare. The conditions for the onset of arrhythmia and the clinical characteristics of VT and Vf patients in exercise stress testing were studied. METHODS: Fifty-nine patients (mean age 54 +/- 17 years, 41 males, 18 females) with VT (succession of 3 or more ventricular premature beats) or Vf induced in exercise stress testing were selected from 7,594 patients with consecutive treadmill stress testing in our hospital from January 1993 to February 1998. RESULTS: The incidence of exercise-induced VT or Vf was 0.8%, and there were no fatal accidents in all tests. Among the 59 patients with exercise-induced VT or Vf, 52 patients had non-sustained VT, 5 had sustained VT, and 2 had Vf. Of the 59 patients, 23 had rhythm or conduction disturbances, 14 had coronary artery disease, 13 had cardiomyopathy, and 9 had valvular heart disease. The VT or Vf incidence in coronary artery disease was 0.2%, and in valvular heart disease was 10.8%. VT or Vf occurred at over 80% of maximum heart rate exercise intensity in 40 patients, including 4 with sustained VT and 2 with Vf, of the 59 patients. Also, in 9 VT patients including the 4 sustained VT patients, VT occurred in the exercise recovery period within 2 min after the exercise. Although VT disappeared spontaneously in 52 non-sustained VT and 3 sustained VT patients, intravenous injection of lidocaine was needed in 2 sustained VT patients and direct current defibrillator was needed in 2 Vf patients. Furthermore, only one non-cardiac death was observed in the follow-up period of average 42 months. CONCLUSIONS: Our results showed clinical characteristics and incidence of VT or Vf similar to past reports. Furthermore, all sustained VT and Vf patients, who should be treated urgently, had a past history of ventricular premature beats or VT. Our data suggest that VT and Vf could occur during the recovery period, especially in patients with documented ventricular tachyarrhythmias when the stress intensity has reached the critical level in the exercise tolerance test.

Aged↗

Detailed activation sequence in the region of electrically induced ventricular fibrillation in dogs.

We determined the details of ventricular activation sequence during the onset of ventricular fibrillation in 6 dogs. Unipolar electrograms were simultaneously recorded from 192 ventricular epicardial sites evenly spaced in a 3 by 3 cm square area surrounding 2 central sites to which stimuli for inducing fibrillation were delivered. In 5 dogs, 2 to 10 msec duration pulses with amplitudes of 150 to 220 v were used to induce fibrillation, and in 1 dog, 3 successive permature stimuli of 3 v intensity were used to induce fibrillation. In 2 dogs the pattern of activation at the onset of fibrillation was compatible with local reentrant paths near the stimulus site. Fibrillation was induced with a single high intensity pulse in both of these dogs. In the other 4 dogs, the pattern of activation at the onset of fibrillation was highly suggestive of reentrant paths distant from the stimulating electrodes. In 3 of these dogs fibrillation was induced by a single high intensity pulse and in the other it was induced by 3 repetitive stimuli. Activation patterns resembling supraventricular activation occurred prior to fibrillation in the latter animal. The data demonstrate 2 distinct modes of onset of electrically induced ventricular fibrillation. The findings support local reentry in the region of the stimulus site as the mode of onset of fibrillation in some animals and possible reentry at sites distant from the stimulus site with participation of the specialized conduction system in other animals. The differences in mode of onset of electrically induced fibrillation may be responsible for instability of fibrillation threshold measurements in some animals. In addition the role of the specialized conduction system in the onset of fibrillation may be responsible for the effects of sympathetic and vagal stimulation on fibrillation threshold.

Animals↗

Reperfusion ventricular fibrillation during coronary artery bypass operations and its association with postoperative enzyme release.

Elevated creatine kinase MB level is the most common marker of myocardial infarction in patients who have had a recent coronary bypass operation. This study was performed to determine whether there is any relationship between reperfusion rhythms, their treatment, and postoperative creatine kinase MB concentrations. Twenty patients were monitored during coronary bypass operations. Four patients had no reperfusion ventricular fibrillation and no elevation of creatine kinase MB postoperatively. Of the 16 remaining patients, all had ventricular fibrillation and 12 had an elevation of postoperative creatine kinase MB (p less than 0.015). There was also a 75% correlation between the time in ventricular fibrillation and postoperative creatine kinase MB level. There was no correlation between other measured parameters, such as cross-clamp time, bypass time, or the number of defibrillations. It is concluded that reperfusion ventricular fibrillation is associated with release of creatine kinase MB, and the time in ventricular fibrillation is correlated with the postoperative creatine kinase MB level.

Aged↗

Myocardial protection during ventricular fibrillation by inhibition of the sodium-hydrogen exchanger isoform-1.

Activation of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) in response to the intense intracellular acidosis that develops during ischemia has been identified as an important mechanism of myocardial cell injury. NHE-1 inhibition in the quiescent (nonfibrillating) heart ameliorates functional manifestation of ischemia and reperfusion injury. We investigated in isolated heart and intact rat models of ventricular fibrillation whether NHE-1 inhibition, by using the selective inhibitor cariporide, could ameliorate myocardial abnormalities that develop during ventricular fibrillation and limit resuscitability and survival. In the isolated rat heart, cariporide significantly reduced the magnitude of ischemic contracture during ventricular fibrillation and the accompanying increases in coronary vascular resistance. Hearts that had received cariporide during ventricular fibrillation had no diastolic dysfunction after resuscitation and recovered their systolic function earlier. In intact rats, cariporide given immediately before starting chest compression allowed generation of a coronary perfusion pressure and end-tidal Pco2 comparable with control rats but with significantly less depth of compression. Cariporide had an unprecedented effect in this rat model, prompting spontaneous defibrillation after approximately 8 mins of chest compression. After resuscitation, rats treated with cariporide had significantly less ventricular ectopic activity, better hemodynamic function, and higher survival rates (22 of 24 [94%] vs. 15 of 24 [63%] in control rats, p <.05). We conclude that NHE-1 inhibition may represent a novel and highly effective form of treatment for resuscitation from ventricular fibrillation.

Animals↗

Pacing-induced ventricular fibrillation leading to oxygen free radical formation in aerobically perfused rat hearts.

The objective of this study was to determine whether electrically-induced ventricular fibrillation can elicit oxygen free radical formation, even in the absence of ischemia and reperfusion. Rat hearts (n = 8 in each group) were perfused aerobically at 37 degrees C and ventricular fibrillation was induced by pacing (20 Hz, 1200 beats/min) for 10 min, during which time no changes in coronary flow rates were observed. In this study, electron spin resonance (ESR) studies using the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) demonstrated the formation of oxygen free radicals consisting of 1:2:2:1 quartet with peak concentration at the 3rd min of fibrillation in non-ischemic electrically fibrillating hearts. Since there were no significant changes in coronary flow rates during ventricular fibrillating (22.3 +/- 1.3 ml/min in control vs 22.3 +/- 0.9 ml/min in pacing-induced fibrillating group), the formation of oxygen free radicals could not be attributed to a pacing-induced ischemic event. In additional studies, hearts were paced by 10 Hz (600 beats/min), to demonstrate whether ventricular tachycardia could elicit free radical formation. In these experiments the genesis of oxygen free radicals was not observable after 1 min, 5 min, and 10 min of tachycardia, but a small amount of OH. radicals was detected at the 3rd min of ventricular tachycardia. When DMPO was infused into the heart giving a final perfusate concentration of 2.5 mmoles/litre during the pacing-induced fibrillation period, myocardial function (aortic flow, cardiac output, left ventricular developed pressure, first derivative of left ventricular developed pressure, and end-diastolic pressure) was significantly improved after the postfibrillating period. In conclusion, our studies clearly show that electrically-induced ventricular fibrillation is capable of eliciting free radical formation even in the absence of ischemia and reperfusion, and the cardioprotective effect of the spin trap is directly originated from its free radical trapping property and not from the other pharmacological activities of DMPO.

Aerobiosis↗

The effect of swimming exercise on spontaneous ventricular defibrillation and ventricular fibrillation threshold in the isolated perfused rat heart.

Effects of swimming exercise training on left ventricular contraction and relaxation, the incidence of spontaneous defibrillation and the ventricular fibrillation threshold were studied in the isolated, perfused rat heart. The heart/body weight ratio was 4.8 +/- 0.4 x 10(-3) in swimmers compared with 3.9 +/- 0.6 x 10(-3) in sedentary controls (p less than 0.0005). The spontaneous heart rate was lower in isolated hearts of trained animals (222 +/- 18 bpm compared with 244 +/- 28, p less than 0.05). Left ventricular systolic pressure was higher in trained hearts and the rate of ventricular relaxation enhanced (p less than 0.05). The ventricular fibrillation threshold was 7.2 +/- 5.2 and 10.8 +/- 6.1 mamp in hearts of swimmers and controls, respectively, the difference not being significant. The incidence of spontaneous defibrillation was not significantly different between the two groups. It is concluded that, while swimming induces cardiac hypertrophy and hemodynamic changes, it neither protects against the induction of ventricular fibrillation nor facilitates spontaneous defibrillation in the isolated, non-ischemic rat heart.

Animals↗

Thyrotoxic periodic paralysis with ventricular fibrillation.

Electrocardiographic conduction disturbances and nonspecific interval changes are not uncommon during hypokalemic periodic paralysis. Although premature ventricular contractions may occur during the paretic episodes associated with hyperkalemic, normokalemic, and hypokalemic periodic paralysis, ventricular tachycardia is rare; to my knowledge, ventricular fibrillation has not been previously reported. In 1977 a 40-year-old man of Puerto Rican descent was resuscitated from ventricular fibrillation and subsequently received a diagnosis of thyrotoxic hypokalemic periodic paralysis. Following thyroid suppression the patient has been asymptomatic; ambulatory ECG monitor, maximal exercise stress test, and echocardiograms have been normal. This case documents the occurrence of ventricular fibrillation in thyrotoxic periodic paralysis.

Adult↗

Life span of ventricular fibrillation frequencies.

The nature and organization of electrical activity during ventricular fibrillation (VF) are important and controversial subjects dominated by 2 competing theories: the wavebreak and the dominant mother rotor hypothesis. To investigate spatiotemporal characteristics of ventricular fibrillation (VF), transmembrane potentials (V(m)) were recorded from multiple sites of perfused rabbit hearts using a voltage-sensitive dye and a photodiode array or a CCD camera, and the time-frequency characteristics of V(m) were analyzed by short-time fast Fourier transform (FFT) or generalized time-frequency representation with a cone-shaped kernel. The analysis was applied to all pixels to track VF frequencies in time and space. VF consisted of blobs, which are groups of contiguous pixels with a common frequency and an ill-defined shape. At any time t, several VF frequency blobs coexisted in the field of view, and the number of coexisting blobs was on average 5.9+/-2.1 (n=8 hearts) as they appeared and disappeared discontinuously with time and were not fixed in space. The life span of frequency blobs from birth to either annihilation or breakup to another frequency had a half-life of 0.39+/-0.13 second (n=4 hearts). The Ca2+ channel blocker nifedipine increased the stability of VF frequencies and reduced the number of frequency blobs progressing to a single frequency. In conclusion, VF consists of dynamically changing frequency blobs, which have a short life span and can be modified by pharmacological interventions, suggesting that VF is maintained by dynamically changing multiple wavelets.

Action Potentials↗

Prolonged sustained ventricular fibrillation without loss of consciousness in patients supported by a left ventricular assist device.

Patients with cardiomyopathy of either ischemic or nonischemic origin are at increased risk for malignant ventricular arrhythmias. Normally sustained ventricular fibrillation (VF) leads to death very rapidly. We report two patients who remained in sustained VF, supported by a left ventricular assist device, for a prolonged period of time. Perfusion pressure through the device was sufficient to allow the patients to remain awake and responsive for several hours while in VF. The cases represent two of the longest reported episodes of sustained VF recorded in awake patients implanted with such devices.

Aged↗

T-wave oversensing by an implantable cardioverter defibrillator after successful ablation of idiopathic ventricular fibrillation.

Focal ablation of trigger premature ventricular complexes (PVCs) from the Purkinje system helped to suppress idiopathic ventricular fibrillation (VF) in an athlete who had suffered from frequent appropriate shock therapies. However, only a few days after successful ablation T-wave oversensing occurred during exercise and resulted in repetitive distressing defibrillator shocks. Despite lack of any changes on the surface ECG, the endocardially recorded electrogram revealed an unfavorable ratio of R-to-T-wave amplitude predisposing to double counting with accelerated heart rates. This case illustrates that T-wave oversensing may complicate the clinical course after successful ablation of malignant Purkinje ectopy.

Adult↗

Prediction of in-hospital ventricular fibrillation from admission data in acute myocardial infarction.

We studied retrospectively 26 readily obtainable clinical and electrocardiographic variables in 22 consecutive patients who experienced primary ventricular fibrillation in association with an episode of acute myocardial infarction. Twenty-eight consecutive patients who had an uncomplicated course after acute myocardial infarction served as controls. The clinical profile of the two groups was similar except that patients who had primary ventricular fibrillation smoked more and had a higher peak creatinine phosphokinase level at the time of infarction. The data was evaluated using univariate and stepwise logistic regression analysis. This analysis demonstrated that patients who developed primary ventricular fibrillation had, on admission (1) more evidence of congestive heart failure (Killip classification), (2) a lower diastolic blood pressure, (3) greater ST-segment elevation, (4) a longer QTc interval, and (5) a less distinguishable J point on the electrocardiogram. This method of logistic analysis that utilizes easily obtainable hospital admission data serves as a preliminary model for prediction of the relative risk of primary ventricular fibrillation in a patient with acute myocardial infarction. The ability to identify patients at risk has important therapeutic implications.

Aged↗