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Biomedical subjects

M M Mower

Publications and source records attributed to M M Mower.

At least 19 recordsLinked to original sources
PubMed1992

The automatic implantable cardioverter-defibrillator. Long-term clinical experience and outcome at a hospital without an open-heart surgery program.

From November 1982 through April 1989, 111 patients with refractory sustained ventricular tachycardia/fibrillation had the automatic cardioverter-defibrillator implanted at our institution, the first community hospital involved in implantation of such a device. We have reviewed our long-term clinical experience to assess the feasibility, learning curve, and efficacy of device implantation in a facility with cardiac electrophysiology expertise but without open-heart surgery facilities. All patients were considered inoperable or at high risk for other concomitant surgery. Eighty-six patients (77%) underwent uneventful implantation. Nine patients (8%) died prior to hospital discharge. Operative mortality declined from 10.9% to 5.4% during the first half (55 patients; November 1982 through September 1986) and second half (56 patients; October 1986 through April 1989) of the experience. Other postoperative complications occurred in 16 patients (14%), 12 of whom experienced complications during the first half of the experience. At 22 +/- 20 (mean +/- SD) months' follow-up, 78 (76%) of 102 patients discharged were alive, and 24 patients (24%) had died. Fifty patients (49%) had experienced at least one automatic cardioverter-defibrillator discharge associated with hypotensive symptoms. The actuarial incidence of sudden death at 1, 2, and 3 years was 1.2%, 5.5%, and 6.2%, respectively. We concluded that the automatic implantable cardioverter-defibrillator is an effective therapy for refractory ventricular tachycardia/fibrillation and that device implantation at community hospitals with an experienced cardiac electrophysiology team is both feasible and practical.

Adult↗
PubMed1992

Case report: myocardial ischemia: an overlooked substrate in syncope of aortic stenosis.

The cause of the syncope in aortic stenosis has been the subject of controversy partly because only a few patients have been monitored during their syncopal episodes. Among the mechanisms proposed are hypersensitive carotid sinus, complete A-V block, ventricular arrhythmias, and ischemic myocardial depression. It is now accepted that the syncope is caused by a vasodepressor response from stimulation of left ventricular baroceptors, resulting in reflex hypotension and bradycardia. This case report describes a patient who developed a syncopal episode during stress testing. Although the mechanism for the syncope is consistent with the vasodepressor response, ischemic changes were observed in the electrocardiogram before the development of syncope. Review of literature shows that, although different mechanisms for syncope have been described, all reported patients manifested myocardial ischemia before the development of their syncopal episodes even when the syncope was nonexertional and clearly caused by a vasodepressor response. The authors conclude that, independent of the mechanism proposed, myocardial ischemia is overlooked as an important substrate in which the syncopes are precipitated in aortic stenosis.

Aged↗
PubMed1992

Automatic implantable cardioverter defibrillator: surgical approaches for implantation.

Surgical approaches for implantation of the automatic cardioverter defibrillator are sternotomy, left thoracotomy, subxiphoid, and subcostal. Although any one of these may be combined with insertion of one or more of the electrodes transvenously, surgical entry into the chest is required for every noninvestigational defibrillator implantation operation. The approaches differ in exposure provided for selecting electrode sites and for handling untoward events, in amount and location of tissue that must be divided or dissected, and in average time required. The operation is an electrical one. Its purpose is to obtain reliable rhythm sensing so that defibrillation or cardioversion shocks will occur only when necessary, and to obtain low enough defibrillation thresholds for shocks of 30 joules or less to have a 10-joule defibrillation safety margin. Many of the patients have had previous cardiac operations. They usually have low or very low ejection fractions. Intraoperative electrophysiological testing with often multiple defibrillation episodes is required. The choice of approach varies with the state of the patient, the institutional experience, and the surgeon. This article describes technique, and the advantages and disadvantages of the four approaches as used by four surgeons in four different institutions.

Defibrillators, Implantable↗
PubMed1991

Effects of pacing rate and timing of defibrillation shock on the relation between the defibrillation threshold and the upper limit of vulnerability in open chest dogs.

To test the relation between the defibrillation threshold and the upper limit of vulnerability, the shock strength associated with 50% probability of successful defibrillation (DFT50) and that associated with 50% probability of reaching the upper limit of vulnerability (ULV50) were determined in 20 open chest dogs with use of the delayed up-down method, with pacing drive cycle lengths of 150 to 500 ms and either single 6-ms shocks (10 dogs) or 12-ms biphasic shocks (10 dogs) given at the mid-upslope, peak and mid-downslope of the T wave of electrocardiographic lead II. The shocks were given by means of a patch-patch configuration on the anterior and posterior surfaces of the heart, which was paced from a stimulating electrode attached to the left ventricular apex. Analysis of variance showed no statistically significant differences in ULV50 as determined with different pacing cycle lengths. For monophasic shocks, DFT50 (331 +/- 66 V or 5.8 +/- 2.7 J) was not significantly different from ULV50 determined at the mid-upslope of the T wave (318 +/- 64 V or 5 +/- 2 J). The correlation coefficients between the two values were 0.74 (p = 0.014) for voltage and 0.67 (p = 0.034) for energy. In contrast, DFT50 was significantly higher than ULV50 as determined at the peak of the T wave (219 +/- 43 V or 2.3 +/- 1 J) and mid-downslope of the T wave (200 +/- 38 V or 1.9 +/- 0.9 J). In three dogs, ventricular fibrillation could not be induced at the mid-downslope of the T wave with any baseline pacing (Si) cycle length.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Clinical efficacy of low energy cardioversion in automatic implantable cardioverter defibrillator patients.

The inclusion of low energy cardioversion capability into modern implantable antiarrhythmic devices, although an appealing idea, is nevertheless unproven with regard to its potential benefits. Moreover, since occasional reports have surfaced suggesting that ineffective application of low energy shocks may prejudice subsequent arrhythmia reversion, we examined the effectiveness and risks of this feature in a large series of patients performed as part of a US Food and Drug Administration clinical trial performed under an investigational device exemption. A total of 813 induced monomorphic ventricular tachycardias were studied in 244 patients. We found that many of the arrhythmias could be reverted to sinus rhythm with small amounts of energy. Cardioversion energy was less than or equal to 6 joules (J) for 84 (53.2%) and less than or equal to 14 joules in 105 (66.4%) of the 158 patients tested at implant and subsequently remained unchanged through greater than 4 months follow up. The incidence of noncardioversion, acceleration or both occurred in 12.7%, 5.7%, and 13.1%, respectively on a per patient basis. On a per episode basis, nonconversion occurred in 51 (6.3%) and acceleration in 61 (7.5%) of the 813 inductions. There was no correlation between the occurrence of nonconversions and accelerations. The devices were allowed to recycle in the event the arrhythmia was not reverted. The subsequent shock was almost always effective, and in any event, no patient failed to be reverted by the second 30-J rescue shock. Over the entire follow-up period as long as 17 months, there were 17 deaths. Neither the incidence nor the mode of death was correlated with nonconversion or acceleration.(ABSTRACT TRUNCATED AT 250 WORDS)

Electric Countershock↗
PubMed1988

Hemodynamic responses to rapid pacing: a model for tachycardia differentiation.

The hemodynamic responses to rapid atrial and ventricular pacing were examined in 10 closed-chest anesthetized dogs in an attempt to distinguish hemodynamically stable from unstable tachycardias. Pressure monitoring catheters were placed in the femoral artery, right atrium, and right ventricle to measure mean arterial pressure, mean right atrial pressure, and mean right ventricular pressure at baseline heart rate and after rapid high right atrial and right ventricular apex pacing. Pressures recorded during rapid pacing (average of the pressures at 30 and 60 seconds of pacing) at pacing rates of 180, 250, and 280/minute were compared to those recorded initially at baseline heart rates. Rapid right ventricular apex pacing resulted in significant increases in mean right atrial pressure (from 6 +/- 1 mmHg (mean +/- standard error) to 12 +/- 1 mmHg, a 100% increase, P less than 0.001) and mean right ventricular pressure (from 11 +/- 1 mmHg to 16 +/- 1 mmHg, a 45% increase, p less than 0.02) with marked hemodynamic compromise (mean arterial pressure decreased from 85 +/- 6 mmHg to 50 +/- 6 mmHg, a 41% decrease, P less than 0.01). These parameters remained stable (no statistically significant difference from baseline) during high right atrial pacing. In half of the dogs high right atrial pacing at rates greater than or equal to 250 resulted in atrioventricular Wenckebach. Thus, it is concluded that mean right atrial pressure and mean right ventricular pressure may be useful in distinguishing hemodynamically significant tachycardias, and in the future design of antitachycardia devices.

Animals↗
PubMed1988

AICD indications (patient selection): past, present and future.

During the course of a seven year implant experience with the Automatic Implantable Cardioverter-Defibrillator (AICD) now extending to well over 3,700 implantees, several functional advances have been made in the pulse generators, and criteria for implantation were successively broadened. Survival statistics have been excellent with 1-year arrhythmic survival over 98%, and total survival from all causes of death in excess of 60% at 5 years. Still, only relatively few of the patients who could possibly be helped by this device actually receive one. Reasons for this are probably complex but include, among other things, the relative newness of electrophysiology as a subspecialty, and a lack of appreciation by the general medical public in regard to this particular treatment modality. Small increases in referral patterns thus can have the potential to produce marked increases in the utilization of AICDs. Additionally, other high risk populations appear to be ready for inclusion into AICD therapeutic trials, and techniques also appear at hand to examine presumably healthy populations so as to predict those subject to suffer eventual sudden cardiac arrest. Under such circumstances, the ultimate impact of AICD therapy can hardly be imagined.

Arrhythmias, Cardiac↗
PubMed1987

Success of chronic defibrillation and the role of antiarrhythmic drugs with the automatic implantable cardioverter/defibrillator.

Because the automatic internal cardioverter defibrillator's long-term ability to reduce arrhythmic mortality in patients with ventricular tachycardia/fibrillation is unknown, it is important to determine whether the threshold for defibrillation changes over time. Serial defibrillation thresholds were measured in 23 patients over a mean replacement time of 24.8 +/- 7.5 months. In all cases the lead system was a superior vena cava coil to a left ventricular epicardial patch. The defibrillation threshold for the entire group increased from 12.3 +/- 4.7 J to 16.9 +/- 5.9 J (p less than 0.05). Striking increases in the defibrillation threshold were seen in the subgroup of patients taking amiodarone (from 10.9 +/- 4.3 J at implantation to 20.0 +/- 4.7 J at replacement, p less than 0.05). Defibrillation threshold decreased in patients taking no antiarrhythmic drugs or taking class I agents. Thus, the increase in mean defibrillation threshold was the result of an increase in the patients taking amiodarone. These data suggest that at initial implantation lead systems associated with the lowest defibrillation threshold should be used and the defibrillation threshold should be measured at generator change to guarantee an adequate margin of safety.

Aged↗
PubMed1987

Sudden cardiac death from acute fluoride intoxication: the role of potassium.

The mechanism of sudden cardiac death following acute fluoride intoxication has been thought to result from profound hypocalcemia produced by the precipitation of calcium fluoride salts. In studies of a canine model, the onset of lethal ventricular arrhythmias was temporally more associated with an elevation of serum potassium than with a drop in serum calcium. Fluoride-induced hyperkalemia could not be prevented with glucose, insulin, or bicarbonate. In the erythrocytes, a five-minute exposure to 10 mM NaF caused a 50% increase in extracellular potassium concentrations after 12 hours compared to control erythrocyte suspensions (P less than .001). The total potassium efflux after 12 hours of incubation was linearly related to the log of fluoride contact time (r, 0.886; P less than .001). The treatment of fluoride-induced hyperkalemia may depend on removal of fluoride and potassium.

Animals↗