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Biomedical subjects

M A Vos

Publications and source records attributed to M A Vos.

At least 55 records · Page 3Linked to original sources
PubMed1994

Inter- and intraindividual variations in shortening of ventricular effective refractory period after an abrupt decrease in pacing cycle length.

After an abrupt decrease in pacing cycle length (PCL), the ventricular effective refractory period (VERP) shortens. The pacing protocol needed to determine accurate and reproducible values for the VERP during this process is elaborate and time consuming. In this study, steady-state values of VERP at 800 and 350 msec PCL and dynamic values of VERP due to an abrupt change in PCL from 800 to 350 msec were determined. This was done for 11 different dogs to test the interindividual variation and repetitively in the same dog to test the intraindividual variation. The results for steady-state and dynamic values of the VERP show a wide range for both groups. This means that accurate prediction of steady-state and dynamic values of VERP based on previous measurements is not possible.

Animals↗
PubMed1994

Is the ventricular effective refractory period different when determined by incremental versus decremental scanning?: the effect of pacing cycle length, d-sotalol, and levcromakalim.

In the clinical setting, the ventricular effective refractory period (VERP) is determined by an 8-beat drive train (S1S1), followed by a premature stimulus (S2), which is decremented in subsequent drive trains until capture is lost. Variation in intertrain pauses and capturing extra stimuli disturb steady-state conditions and reduce reproducibility of values found for the VERP. To increase reproducibility, a protocol without intertrain pause and incremental scanning (IS) of S2 was developed. In anesthetized dogs with chronic AV block, determination of the VERP using IS and decremental scanning (DS) without intertrain pause was compared at 800 and 350 msec pacing cycle length (PCL). The measurements were repeated after the administration of d-sotalol to lengthen the VERP and levcromakalim to shorten the VERP. The results showed no difference between IS and DS at both PCLs with or without medication. Recurrent and abrupt rate changes were avoided during IS, making this the protocol of choice when induction of arrhythmias is to be avoided.

Animals↗
PubMed1994

Mechanism-specific antiarrhythmic effects of the potassium channel activator levcromakalim against repolarization-dependent tachycardias.

INTRODUCTION: The hypothesis that levcromakalim, a potassium channel (IK-ATP) activator with antihypertensive properties, has a mechanism-specific antiarrhythmic action against repolarization-dependent ventricular tachycardias (VTs) was tested in dogs. METHODS AND RESULTS: A low dose of levcromakalim (0.01 mg/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (1) d-sotalol (2 mg/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs), (2) sustained ouabain-induced VTs, which are dependent on delayed afterdepolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d-sotalol induced U waves, ventricular ectopic beats, and self-terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d-sotalol from 1490 +/- 515 to 1700 +/- 610 msec (P < 0.05), remained similar after levcromakalim (1655 +/- 580 msec). The QT(U) duration, which was increased after d-sotalol from 410 +/- 55 to 550 +/- 40 msec (P < 0.05), normalized to 405 +/- 70 msec (P < 0.05). Levcromakalim did not suppress but rather enhanced ouabain-induced VT by decreasing the cycle length slightly from 315 +/- 35 to 290 +/- 35 msec (P < 0.05). Pretreatment with a beta blocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction. CONCLUSION: A low dose of levcromakalim has specific antiarrhythmic properties against repolarization-dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.

Animals↗
PubMed1993

Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris.

The aim of this study was to assess the value of the electrocardiogram recorded during chest pain for identifying high-risk patients with 3-vessel or left main stem coronary artery disease (CAD). Therefore, the number of leads with abnormal ST segments, the amount of ST-segment deviation, and specific combinations of leads with abnormal ST segments were correlated with the number of coronary arteries with proximal narrowing of > 70%. Electrocardiograms recorded during chest pain were compared with one from a symptom-free episode. In this retrospective analysis, 113 consecutive patients were included. One-vessel CAD was present in 47 patients, 2-vessel CAD in 22, 3-vessel CAD in 24 and left main CAD in 20. Stratification was performed according to the presence of an old myocardial infarction. The number of leads with ST-segment deviations, and the amount of ST-segment deviation in the electrocardiogram obtained during chest pain at rest showed a positive correlation with the number of diseased coronary arteries. These findings were more marked when the absolute shifts from baseline were considered, because ST-segment abnormalities could be present also in the electrocardiogram obtained during the symptom-free episode. Left main and 3-vessel CAD showed a frequent combination of leads with abnormal ST segments: ST-segment depression in leads I, II and V4-V6, and ST-segment elevation in lead aVR. The negative predictive and positive accuracy of this pattern were 78 and 62%, respectively. When the total amount of ST-segment changes was > 12 mm, the positive predictive accuracy for 3-vessel or left main stem CAD increased to 86%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

R56865, an antiarrhythmic drug with class III effects that terminates ouabain induced ventricular tachycardia in an inverse rate dependent manner.

OBJECTIVE: R56865 has been described as a substance that protects cells from intracellular Na+ and Ca2+ overload. The aim of this study was to investigate its mechanism of action, which is at present unknown. METHODS: The haemodynamic and (rate dependent) electrophysiological effects of R56865 (0.48 mg.kg-1) were examined and compared with its antiarrhythmic effect on ouabain-induced ventricular tachycardia (n = 10), and ventricular tachycardia occurring within 24 h of occlusion of the left anterior descending artery (n = 8). The experiments were all performed in dogs. RESULTS: In anaesthetised dogs R56865 increased (p < 0.05) the cycle length of the sinus rhythm, the corrected QT duration (+8%) and the effective refractory period (+16%) of the right ventricle. No rate dependency was found. R56865 had no effect on blood pressure, conduction, or refractoriness of the AV node, nor on conduction in the ventricle. In conscious dogs, R56865 did not change the cycle length of the sinus rhythm, but it did increase the QT duration (+5%, p < 0.05). The cycle length of the slower ouabain induced ventricular tachycardias which were terminated by R56865 increased to a greater extent (+55%) than that of the non-suppressible, faster ventricular tachycardias (+16%): 335(SD 30) ms, n = 5 v 285(10) ms, n = 5. The effect of R56865 on ventricular tachycardias 24 h after infarction was considered to be of minor antiarrhythmic importance. CONCLUSIONS: R56865 has (1) class III effects, (2) a partial effect in terminating ouabain induced ventricular tachycardias which is inverse rate dependent, and (3) a weak effect on ventricular tachycardias 24 h after infarction.

Animals↗
PubMed1993

Effects of magnesium and ethmozin on ventricular tachycardia induced by ouabain and ventricular pacing in conscious dogs with complete atrioventricular block.

A study was made of whether the administration of magnesium or ethmozin to conscious dogs with normal plasma Mg levels (0.75 +/- 0.06 mmol/l) terminates ouabain-induced ventricular tachycardia, an arrhythmia which is dependent on triggered activity resulting from delayed afterdepolarizations. Sustained monomorphic ventricular tachycardia was induced by programmed ventricular pacing during the continuous iv. infusion of ouabain to animals with a formaldehyde-induced permanent complete AV block. A single dose of MgSO4 (100 mg/kg b.w. iv.) abolished only those ventricular tachycardias with cycle lengths > 325 ms (inverse use-dependency); ventricular tachycardias with cycle lengths < 320 ms were merely slowed, despite the fact that the increase in plasma Mg levels was considerable and comparable in both groups (3.9 +/- 1.6 and 4.8 +/- 1.9 mmol/l). In contrast, ethmozin (2 mg/kg b.w. iv.) terminated both fast and slow ventricular tachycardias. It is concluded that ethmozin (moricizine) is more effective than the traditionally used MgSO4 in terminating ventricular tachycardia resulting from cardiac glycoside toxicity.

Animals↗
PubMed1992

Ventricular arrhythmias in heart failure.

Heart failure is an increasingly common disorder leading to reduced quality and expectancy of life. Asymptomatic and symptomatic ventricular arrhythmias are a frequent complication and have been found to be independent prognostic predictors for sudden cardiac death in patients with heart failure. Unfortunately, the positive predictive failure for this finding is low, but in patients with sustained ventricular arrhythmias, variables indicating impaired pump function are the most important predictors of sudden and of nonsudden cardiac death. Arrhythmias in heart failure may have many different underlying mechanisms. Indications for, and mode of treatment of, arrhythmias in heart failure depend on the symptoms and prognostic significance of the arrhythmia. Primarily, pump function should be optimized and antiarrhythmic drug therapy instituted only when the arrhythmia persists. In poorly tolerated and life-threatening arrhythmias, implantable devices allowing pacing and defibrillation must be considered. No data are presently available indicating a protective role of antiarrhythmic drugs in the prevention of sudden cardiac death in heart failure. Future directions should concentrate on the development of better stratification of risk for sudden death, better delineation of mechanisms of arrhythmias in heart failure (allowing the development of mechanism-specific antiarrhythmic drugs), and research into new nonpharmacologic techniques such as cardiomyoplasty and molecular biologic techniques to rebuild the failing heart muscles.

Arrhythmias, Cardiac↗
PubMed1992

Programmed electrical stimulation and drugs identify two subgroups of ventricular tachycardias occurring 16-24 hours after occlusion of the left anterior descending artery.

BACKGROUND: Spontaneous sustained ventricular tachycardia (VT) occurring 16-24 hours after left anterior descending (LAD) coronary artery occlusion in the canine heart is most likely based on abnormal automaticity. In vitro, it has been demonstrated that the rate of the arrhythmia and the effect of overdrive pacing depends on the maximal diastolic potential (MDP). The MDP is also of importance in understanding the effect of antiarrhythmic drugs. To study 1) the possible presence of different responses to overdrive pacing and 2) the relation between the response to overdrive pacing and the effect of different antiarrhythmic drugs in the intact heart, we investigated the effect of 1) (prolonged) pacing and 2) lidocaine (3 mg/kg), verapamil (0.4-1.0 mg/kg), or flunarizine (2 mg/kg) during VT. METHODS AND RESULTS: In 21 conscious dogs with chronic atrioventricular block, 60 sustained VTs were observed 1 day after LAD occlusion. During VT, pacing with interstimulus intervals of 400, 300, and 200 msec for 15, 60, and 120 seconds was done on 40 VTs. Based on their response to pacing, VTs were divided into a pacing-suppressible (PS group) and a pacing-nonsuppressible group (PNS group). The mean cycle length in the PS group was significantly longer (410 +/- 50 msec) than in the PNS group (360 +/- 35 msec, p less than or equal to 0.01). Suppression was directly related to the rate and duration of pacing. Spontaneous recurrence of VTs was observed after 26 +/- 45 seconds. Lidocaine and verapamil increased cycle length of the suppressible VTs and terminated them, whereas flunarizine had no effect. Except for verapamil, which increased cycle length of the VTs, no effects were seen in the PNS group. CONCLUSIONS: In conscious dogs showing sustained VTs 16-24 hours after LAD occlusion, 1) the slower VTs can be suppressed by pacing, verapamil, and lidocaine but not by flunarizine, and 2) the faster VTs are not affected by pacing, lidocaine, and flunarizine, and are only slowed by verapamil. These findings are compatible with in vitro findings of abnormal automaticity, with the slower VTs originating from a higher MDP than the faster VTs.

Animals↗
PubMed1992

Further observations to confirm the arrhythmia mechanism-specific effects of flunarizine.

In conscious dogs with chronic atrioventricular (AV) block, we recently demonstrated that flunarizine is effective against ouabain-induced arrhythmias (triggered activity resulting from delayed afterdepolarizations, DADs) but fails to suppress spontaneous ventricular tachycardias (VT) occurring 24 h after left anterior descending coronary artery occlusion (abnormal automaticity). Neither does flunarizine affect normal automaticity, which suggests that flunarizine could be used as a clinical tool to recognize cardiac arrhythmias based on triggered activity. To elucidate further the arrhythmia mechanism-specific action of flunarizine, we investigated (a) its hemodynamic and electrophysiologic effects in 6 anesthetized dogs, (b) its ability to prevent pacing-induced VT 7 days after myocardial infarction (reentry) in 9 anesthetized animals, and (c) its effect on premature escape beats (PEBs) in 9 conscious dogs with chronic AV block. PEBs are probably caused by DADs. Flunarizine decreased systemic blood pressure (p less than 0.01), and left ventricular dP/dt (p less than 0.01), but did not affect AH or HV internal, QRS duration, QT time, or the effective refractory period of either AV node or right ventricle over a wide range of (paced) cycle lengths. Flunarizine decreased the inducibility of PEBs by 42% (p less than 0.01), but not that of the reentrant VT in any of the 6 inducible dogs. Therefore, we conclude that although flunarizine has no electrophysiologic effects in normal heart, it prevents induction of PEBs. The inability of flunarizine to prevent induction of reentrant VT confirms the mechanism-specific action of flunarizine against triggered activity.

Analysis of Variance↗
PubMed1991

Significance of the number of stimuli to initiate ouabain-induced arrhythmias in the intact heart.

Ouabain-induced arrhythmias are a well-known model used to study triggered activity resulting from delayed afterdepolarizations. In the intact heart, initiation of these arrhythmias is promoted by pacing, especially at fast rates. However, the relevance of the number of stimuli is unknown. In conscious dogs with formalin-induced atrioventricular block, we investigated the effect of variations in pacing mode on 1) the behavior of nonsustained triggered rhythms at progressive levels of ouabain intoxication, and 2) the induction of sustained ventricular tachycardia (VT). Twenty experiments were analyzed. Ouabain was administered as a bolus of 40 micrograms/kg followed by continuous infusion. Every 15 minutes the pacing protocol was repeated, with a maximum of 10, until completion or induction of VT. When VT could not be initiated, the experiment was repeated at least 1 week later, adding 5-10 micrograms/kg ouabain to the bolus and increasing the infusion rate correspondingly. This was repeated until VT could be induced. Four interstimulus intervals (200, 400, 600, and 800 msec) and seven numbers of stimuli (5, 10, 20, 35, 50, 100, and 150) were given in two pacing protocols. The effect of these protocols on 1) the number of induced beats per stimulation train, 2) their first postpacing interval, and 3) induction of VT were studied. Initiation of VT occurred after 75 +/- 42 minutes. The bolus of ouabain needed to induce VT was inversely related to the body weight of the animals. Progression of ouabain intoxication resulted in 1) a significant increase in the number of induced beats per stimulation train and 2) a significant shortening of the first postpacing interval. Stimulation at a faster rate and/or more stimuli resulted in 1) a significantly pronounced increase in the number of induced beats at the higher levels and 2) a significantly shorter first postpacing interval at successive levels of ouabain intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The in vivo response of ouabain-induced arrhythmias to pacing: acceleration instead of termination.

In vitro, arrhythmias that result from triggered activity based on delayed afterdepolarizations can be reproducibly terminated by pacing. We studied the effect of similar pacing protocols on ouabain-induced ventricular tachycardia (VT) in the intact canine heart. The experiments were performed in 17 conscious dogs that had surgically induced atrioventricular block. The pacing protocol included 1, 2, or 20 stimuli and also continuous stimulation during 15, 60, and 120 seconds with interstimulus intervals varying between 500 and 200 msec. A total of 331 stimulation trains were given. The cycle length of the ouabain-induced VT was compared before and after pacing. The mean R-R interval of the induced VT was 380 +/- 80 msec. Termination was only observed in 3% of the pacing experiments and was not reproducible. The common response to pacing was a shortening in cycle length of VT that resulted in R-R intervals of 300 +/- 50 msec (p less than or equal to 0.001). Acceleration was dependent on duration of stimulation. A decrease in the interstimulus interval resulted in shortening of both the first postpacing interval and the cycle length of VT after pacing. These concordant relations were independent of the pacing modes. In conclusion, pacing of ouabain-induced VT in the intact heart rarely results in termination of the arrhythmia. Acceleration of VT is the rule. This finding may be of help in differentiating triggered activity that results from delayed afterdepolarizations from other arrhythmogenic mechanisms.

Animals↗
PubMed1990

Flunarizine allows differentiation between mechanisms of arrhythmias in the intact heart.

The calcium antagonist flunarizine suppresses pathologic accumulation of calcium intracellularly without affecting the fast sodium or the slow calcium channel. To establish its value in differentiating between mechanisms of arrhythmias in the canine heart, the effect of flunarizine was investigated on ventricular tachycardia (VT) induced by ouabain intoxication or occurring 16-24 hours after occlusion of the left anterior descending coronary artery. Four groups of dogs were studied. Group 1 consisted of 13 animals with VT induced by ouabain intoxication (triggered-activity group). Group 2 included nine dogs in whom VT developed 16-24 hours after occlusion of the left anterior descending coronary artery (abnormal automaticity group). Group 3 included six dogs with normally conducted sinus beats, whereas group 4 consisted of six animals having a ventricular escape rhythm. With the exception of group 3, all dogs had surgically induced complete atrioventricular block. All animals were studied while conscious and without premedication. In groups 1 and 2, 2-3 mg/kg flunarizine was given intravenously after VT had persisted for at least 20 minutes. In groups 3 and 4, 2 mg/kg flunarizine was given after the rhythm was registered for 20 minutes. The cycle lengths of the different rhythms were compared before and after flunarizine. In group 1, flunarizine increased the cycle length of the VT from 300 +/- 30 to 410 +/- 50 msec (p less than or equal to 0.001). Termination of VT was seen in 11 out of 13 animals. In group 2, flunarizine resulted in a nonsignificant shortening of the RR interval from 450 +/- 60 to 440 +/- 60 msec. Persistent termination was observed in only one of nine dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Premature escape beats. A model for triggered activity in the intact heart?

In conscious dogs with complete atrioventricular block, overdrive pacing of the idioventricular rhythm normally results in overdrive suppression (OS). Frequently, however, we observed another response to overdrive, that is, QRS complex or complexes with unexpectedly short coupling intervals followed by normal OS. We have named such a QRS complex a "premature escape beat" (PEB). Based on the response of PEBs to electrical stimulation, we postulate that PEBs are based on triggered activity resulting from delayed afterdepolarizations. This hypothesis was tested in 82 experiments by 1) stimulation under control conditions and in combination with 2) subtoxic and toxic amounts of ouabain 20-50 micrograms/kg, 3) lidocaine 3 mg/kg, and 4) doxorubicin 16-24 mg/m2. The stimulation protocol, which was repeated at random five to 10 times, consisted of 10 and 50 stimuli using interstimulus intervals of 200, 400, 600, and 800 msec. This protocol was not only performed during spontaneous idioventricular rhythm but also during a continuously paced rhythm with interstimulus intervals of 800 msec. It was found that 1) the chance to induce a PEB or PEBs increased and 2) their first postpacing interval significantly decreased using short or fast drives, or both. Ouabain increased significantly and in a dose-dependent manner 1) the ability to induce PEBs and 2) the number of PEBs per stimulation-train, and also shortened their first postpacing interval. Opposite effects were seen after lidocaine, doxorubicin, and continuous pacing as follows: 1) a lower incidence of PEBs and 2) lengthening of their first postpacing interval. These results support our hypothesis that PEBs are based on triggered activity resulting from delayed afterdepolarizations.

Animals↗
PubMed1989

Termination of ouabain-induced ventricular tachycardia by flunarizine in conscious dogs.

The ability of flunarizine to terminate ouabain-induced ventricular tachycardia was investigated in conscious dogs. These arrhythmias result from triggered activity based on delayed afterdepolarizations. Sustained ventricular tachycardia was induced by ouabain (48 +/- 6 micrograms/kg) and pacing in 13 animals with surgically induced complete atrioventricular block. Flunarizine was administered i.v. when the arrhythmia had persisted for at least 20 min. Flunarizine induced an increase of the R-R interval from 300 +/- 30 to 410 +/- 50 ms (P less than or equal to 0.001) in all dogs. Flunarizine (2 mg/kg) terminated ventricular tachycardia with long R-R intervals (330 +/- 20 ms) in seven dogs. An additional dose of flunarizine (1 mg/kg) resulted in termination of the faster tachycardias (280 +/- 15 ms). The arrhythmias were not induced again by pacing for 27 +/- 18 min. Reinitiated tachycardias could be suppressed again by flunarizine. In conclusion, flunarizine (1) slows and terminates arrhythmias resulting from delayed afterdepolarizations, and (2) prevents their reinitiation.

Animals↗
PubMed1989

The effect of an entrainment protocol on ouabain-induced ventricular tachycardia.

Overdrive stimulation of reentrant ventricular tachycardias (VT) may result in entrainment and/or termination of these arrhythmias. We investigated whether surface ECG criteria of entrainment can also be observed in nonreentrant VT. For this purpose ouabain-induced tachycardias were used that are considered to be based on delayed afterdepolarizations. In nine conscious dogs, having surgically induced complete AV block, pacing was performed using trains of 20 stimuli from a site distant to the origin of the VT. The pacing intervals were shortened in steps of 5-10 msec, until complete capture from the pacing site or termination of the VT was obtained. During stimulation variable fusion was seen and complete capture of the ventricles from the pacing site occurred just after a slight decrease in pacing cycle length (20 +/- 10 msec). Overdrive stimulation resulted only in 1 out of 58 stimulation trains in termination of VT. Following stimulation it was observed that: (1) The length of the first postpacing interval was significantly longer (P less than 0.001) than both the mean prepacing VT cycle length and interstimulus interval; (2) A change in QRS configuration occurred after 57% of the stimulation trains; (3) The VT accelerated slightly in comparison to the prepacing rate (P less than 0.05); and (4) The length of the first postpacing interval and the mean R-R interval of the VT postpacing were directly related to the interstimulus interval (r = 0.82 and 0.97, respectively). In conclusion, overdrive stimulation of ouabain-induced arrhythmias did not result in entrainment or in termination of the tachycardia. Instead, other responses were seen that may be of help in differentiating between arrhythmias caused by delayed afterdepolarizations and reentry.

Animals↗
PubMed1988

Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction.

The value of the accelerated idioventricular rhythm (AIVR) as a marker for myocardial necrosis and/or reperfusion was prospectively studied in 87 patients admitted with persistent ischemic chest pain. All patients received streptokinase. Necrosis was diagnosed by new Q waves and an increase in plasma enzymes. Reperfusion was documented angiographically. Myocardial necrosis occurred in 72 patients and reperfusion in 70 patients, 58 of whom had myocardial necrosis. Of 27 patients with AIVR, 26 had both necrosis and reperfusion (p less than 0.001). AIVR started after a long coupling interval to the preceding sinus rhythm and was regular. Configuration depended on the reperfused infarct vessel. Reperfusion of the left anterior descending branch showed most configurations of AIVR and with the least QRS width. Reperfusion of the circumflex branch never had a left bundle branch block-like configuration. AIVR from reperfusion of the right coronary artery never had an inferior axis. AIVR occurring during persistent ischemic chest pain is a marker for both myocardial necrosis and reperfusion of the infarct vessel. AIVR starts with a long coupling interval and is regular. The QRS configuration may be useful for the noninvasive identification of the infarct vessel.

Aged↗