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Biomedical subjects

G C Flaker

Publications and source records attributed to G C Flaker.

At least 37 records · Page 2Linked to original sources
PubMed1995

Effect of infarct artery patency on prognosis after acute myocardial infarction. The Survival and Ventricular Enlargement Investigators.

BACKGROUND: In patients with acute myocardial infarction (MI), early restoration of patency of the infarct-related artery (IRA) leads to preservation of left ventricular function and improved clinical outcome. However, there is evidence that the benefits associated with a patent IRA are out of proportion to the observed improvement in ventricular function and may result not only from salvage of ischemic myocardium but also from the opening of the IRA beyond a narrow postinfarct time window. The objectives of this study were (1) to assess the effect of IRA patency on outcome of patients after acute MI with left ventricular dysfunction while controlling for differences in left ventricular ejection fraction and the extent of coronary disease and (2) to determine the effect of angiotensin-converting enzyme (ACE) inhibitor therapy on patients with patent as well as occluded infarct arteries. METHODS AND RESULTS: The Survival and Ventricular Enlargement (SAVE) study consisted of 2231 patients with a documented MI and a left ventricular ejection fraction < or = 40%. They were randomized to the ACE inhibitor captopril (50 mg TID) or placebo 3 to 16 days after MI and were followed for an average of 3.5 years. Left ventricular ejection fraction, measured with radionuclide left ventriculography, was repeated at the end of the follow-up period. The 946 patients in whom the patency of the IRA was established before randomization form the basis of this study. At cardiac catheterization averaging 4.2 days after infarction, 30.7% of patients had an initially occluded IRA. After revascularization, 162 of the 946 patients (17.1%) were left with an occluded IRA at the time of randomization. The 162 patients with persistently occluded IRAs and 784 with patent IRAs had similar clinical baseline characteristics, but those with occluded arteries had a slightly lower ejection fraction than the 784 patients with patent infarct arteries (30% versus 32%, P = .01). Cox proportional-hazards analyses showed that the independent predictors of all-cause mortality were hypertension (relative risk [RR] 1.94, P < .001), number of diseased coronary arteries (RR 1.68, P < .001), occluded IRA (RR 1.49, P = .039), ejection fraction (RR 1.36, P < .001), age (RR 1.10, P = .030), and use of beta-adrenergic receptor blocking agents (RR 0.60, P = .007). Independent predictors of a composite end point consisting of cardiovascular mortality, morbidity, or reduction of ejection fraction of > or = 9 units were occluded IRA (odds ratio [OR] 1.73, P = .002), hypertension (OR 1.71, P < .001), number of diseased vessels (OR 1.38, P < .001), ejection fraction (OR 1.18, P = .003), use of beta-adrenergic receptor blocking agents (OR 0.67, P = .007), and randomization to captopril (OR 0.70, P = .009). CONCLUSIONS: IRA patency within 16 days after MI predicts a favorable clinical outcome, independent of the number of obstructed coronary arteries or of left ventricular function. The beneficial effect of ACE inhibition is independent of patency status of the IRA. These findings support the need for additional, prospective clinical trials of late reperfusion in MI patients.

Adrenergic beta-Antagonists↗
PubMed1995

Clinical and echocardiographic features of intermittent atrial fibrillation that predict recurrent atrial fibrillation. Stroke Prevention in Atrial Fibrillation (SPAF) Investigators.

In addition to antithrombotic therapy, 2 treatment strategies for intermittent atrial fibrillation (AF) are evolving: suppression of AF or control of the ventricular response during AF. Clinical and echocardiographic features that predict recurrent AF may influence the choice of management. In this study, clinical, echocardiographic, and electrocardiographic data from 486 patients with intermittent AF enrolled in the Stroke Prevention in Atrial Fibrillation studies were analyzed. Patients with intermittent AF were younger (p < 0.001), had fewer incidences of systemic hypertension (p < 0.007) and heart failure (p < 0.001), and had more recent-onset AF than patients with constant AF. They also had a smaller mean left atrial diameter, a lower prevalence of a large (> 5 cm) left atrium, better left ventricular performance by echo, and less mitral regurgitation. After a mean follow-up of 26 months, 51% of patients remained in sinus rhythm and 49% of patients developed recurrent AF, including 12% who had AF, as seen on all follow-up electrocardiograms. Clinical factors predicting recurrent AF were age, heart failure, and myocardial infarction. An enlarged left atrium was associated with recurrent intermittent AF; an enlarged left ventricle predicted conversion to constant AF. Thus, clinical and echocardiographic parameters predict recurrent AF in patients with intermittent nonvalvular AF.

Age Factors↗
PubMed1995

Angiographic predictors of reocclusion after thrombolysis: results from the Thrombolysis in Myocardial Infarction (TIMI) 4 trial.

OBJECTIVES: This study attempted to determine which lesion characteristics are associated with reocclusion by 18 to 36 h. BACKGROUND: Reocclusion of the infarct-related artery after successful reperfusion is associated with significant morbidity and up to a threefold increase in mortality. METHODS: Two hundred seventy-eight patients with acute myocardial infarction were randomized to receive either anisoylated plasminogen streptokinase activator complex (APSAC) or recombinant tissue-type plasminogen activator (rt-PA) or their combination. Culprit arteries were assessed for Thrombolysis in Myocardial Infarction (TIMI) flow grade, lesion ulceration, thrombus, collateral circulation and eccentricity. Minimal lumen diameter, percent diameter stenosis and lesion irregularity (power) were calculated using quantitative angiography. RESULTS: Reocclusion was observed more frequently in arteries with TIMI 2 versus TIMI 3 flow (10.4% vs. 2.2%, p = 0.003), in ulcerated lesions (10.7% vs. 3.0%, p = 0.009) and in the presence of collateral vessels (18.2% vs. 5.6%, p = 0.03). Similar trends were observed for eccentric (7.3% vs. 2.3%, p = 0.06) and thrombotic (8.4% vs. 3.3%, p = 0.06) lesions. Reocclusion was associated with more severe mean percent stenosis (77.9% vs. 73.9%, p = 0.04). Lesion length, reference segment diameter and Fourier measures of lesion irregularity were not associated with reocclusion. CONCLUSIONS: Several simply assessed angiographic variables, such as the presence of TIMI grade 2 flow, ulceration, collateral vessels and greater percent diameter stenosis at 90 min after thrombolytic therapy, are associated with significantly higher rates of infarct-related artery reocclusion by 18 to 36 h and may aid in identifying the subset of patients who are at significantly higher risk of early reocclusion and who potentially warrant further early pharmacologic or mechanical intervention.

Adult↗
PubMed1994

Use of a standardized heparin nomogram to achieve therapeutic anticoagulation after thrombolytic therapy in myocardial infarction. TIMI 4 investigators. Thrombolysis in Myocardial Infarction.

BACKGROUND: The recently completed Thrombolysis in Myocardial Infarction (TIMI) 4 Study compared three thrombolytic treatment regimens for acute myocardial infarction. The treatment arms included front-loaded recombinant tissue plasminogen activator (rtPA), anistreplase (APSAC), or both, in conjunction with an intravenous bolus of 5000 U of heparin, followed by 1000 U/h. To facilitate anticoagulation, a heparin nomogram was developed to maintain the therapeutic activated partial thromboplastin time at 1 1/2 to 2 times the control value. METHODS: A poll revealed that nine centers made use of the recommended heparin nomogram and six did not, adjusting the heparin dosage according to local practice. Anticoagulation parameters, major hemorrhagic events, and the frequency of heparin interruption were compared between centers that used and did not use the nomogram. RESULTS: Subtherapeutic activated partial thromboplastin time values were noted in 4%, 14%, 29%, 46%, 37%, and 34% of patients 8, 12, 24, 48, 72, and 96 hours, respectively, after heparin treatment was begun. Patients with subtherapeutic values at 24 hours were younger (mean +/- SD, 55.2 +/- 10.6 vs 59.6 +/- 10.6 years, P = .02) and weighed more (86.4 +/- 13.5 vs 78.9 +/- 15.7 kg, P = .007) than patients with therapeutic values. Centers that used the nomogram had significantly fewer subtherapeutic values at 48 and 96 hours. In addition, heparin therapy was interrupted less frequently at centers that used the nomogram (38.1% vs 68.7%, P < .001). Major spontaneous hemorrhage, reinfarction, and reocclusion rates were low and were about the same in the two groups. CONCLUSIONS: The use of a heparin nomogram provided improved anticoagulation in patients treated with thrombolytic therapy for myocardial infarction. Weight- and age-adjusted heparin dosing may provide further improvement in anticoagulation with heparin therapy. Our findings support the need for frequent monitoring of the activated partial thromboplastin time and for a standardized approach to adjusting the heparin dosage.

Aged↗
PubMed1994

Causes of higher in-hospital mortality in women than in men after acute myocardial infarction.

Clinical, laboratory and cardiac catheterization parameters were reviewed in 355 men and 155 women hospitalized at a tertiary care referral center between February 1987 and December 1991 to analyze why women have a higher in-hospital mortality rate than do men after acute myocardial infarction. Hospital mortality was 21.4% in women and 12.1% in men (p = 0.007). In comparison with men, women were older (63.3 +/- 11.9 vs 60.5 +/- 12.6 years; p = 0.023), had more systemic hypertension (46.5 vs 34.4%; p = 0.001) and higher serum total cholesterol levels (211 +/- 51 vs 197 +/- 49 mg/dl; p = 0.0015), sought medical care later (8.9 vs 5.3 hours; p = 0.026), were referred later (47.7 vs 43.7 hours; p = 0.063) and had more shock (34.8 vs 24.2%; p = 0.013). Logistic regression analysis revealed 5 variables predictive of hospital mortality; age > 65 years, diabetes, shock, non-Q-wave infarction, and not undergoing cardiac catheterization. Gender was of borderline significance in predicting hospital mortality. Cardiac catheterization, performed in 88% of women and 87% of men, showed similar rates of 1-, 2- and 3-vessel disease, and similar characteristics of the infarction-related artery. The differences in hospital mortality between men and women are due to a combination of pre- and in-hospitalization factors in women. The excess mortality is not due to differences in disease severity as evaluated by cardiac catheterization information.

Age Factors↗
PubMed1994

Effects of captopril on ischemic events after myocardial infarction. Results of the Survival and Ventricular Enlargement trial. SAVE Investigators.

BACKGROUND: In the Survival and Ventricular Enlargement (SAVE) trial, recurrent myocardial infarction (MI) was the most important predictor of a poor outcome and conferred a sevenfold increase in risk of death. The purpose of this study was to determine the predictors of recurrent MI in study participants and to examine the influence of the angiotensin-converting enzyme inhibitor captopril on this and other myocardial ischemic events. METHODS AND RESULTS: The 2231 patients had survived the acute phase of MI (3 to 16 days) and had a radionuclide ventricular ejection fraction < or = 40%. Patients were randomly assigned to receive double-blind treatment with either placebo or captopril and were followed for an average of 42 months. The influence of captopril on recurrent MI, cardiac revascularization procedures, and hospitalization with unstable angina was examined. The likelihood of recurrent MI was greater in patients with an MI or functional disability before the index infarction and higher systolic pressure (all P < .001) but was not influenced by baseline left ventricular ejection fraction. Therapy with captopril reduced the risk of development of recurrent MI by 25% (95% confidence intervals, 5% to 40%; P = .015) and the risk of death after recurrent MI by 32% (95% confidence intervals, 4% to 51%; P = .029). Captopril-assigned patients were also less likely to require cardiac revascularization procedures (P = .010), but hospitalization for unstable angina was unaltered. When all three of these major coronary ischemic events were considered together, captopril therapy reduced the risk (14% risk reduction; 95% confidence intervals, 0% to 26%; P = .047). CONCLUSIONS: In post-MI patients with asymptomatic left ventricular dysfunction, long-term administration of captopril reduced recurrence of MI and the need for cardiac revascularization but had no influence on the rate of hospitalization with a discharge diagnosis of unstable angina. The finding that the recurrence of MI was independent of left ventricular ejection fraction suggests that captopril could be useful in preventing recurrent MI in patients with more preserved left ventricular function. The need for cardiac revascularization was reduced in patients receiving long-term captopril therapy, suggesting either an anti-ischemic effect or the ability of the angiotensin-converting enzyme inhibitor to modify the atherosclerotic process in survivors of MI.

Angina, Unstable↗
PubMed1993

Prevention of myocardial reinfarction. Recommendations based on results of drug trials.

Therapy after acute myocardial infarction offers the prospect of increased survival in carefully selected patients. Current recommendations favor the use of beta blockers and antiplatelet agents, but some positive effects have been seen with use of anticoagulants, angiotensin-converting enzyme inhibitors, and calcium channel blockers. Further studies are needed to evaluate these drug classes in reinfarction prophylaxis and to define differences among the agents in each class.

Adrenergic beta-Antagonists↗
PubMed1992

Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators.

BACKGROUND: Left ventricular dilatation and dysfunction after myocardial infarction are major predictors of death. In experimental and clinical studies, longterm therapy with the angiotensin-converting--enzyme inhibitor captopril attenuated ventricular dilatation and remodeling. We investigated whether captopril could reduce morbidity and mortality in patients with left ventricular dysfunction after a myocardial infarction. METHODS: Within 3 to 16 days after myocardial infarction, 2231 patients with ejection fractions of 40 percent or less but without overt heart failure or symptoms of myocardial ischemia were randomly assigned to receive doubleblind treatment with either placebo (1116 patients) or captopril (1115 patients) and were followed for an average of 42 months. RESULTS: Mortality from all causes was significantly reduced in the captopril group (228 deaths, or 20 percent) as compared with the placebo group (275 deaths, or 25 percent); the reduction in risk was 19 percent (95 percent confidence interval, 3 to 32 percent; P = 0.019). In addition, the incidence of both fatal and nonfatal major cardiovascular events was consistently reduced in the captopril group. The reduction in risk was 21 percent (95 percent confidence interval, 5 to 35 percent; P = 0.014) for death from cardiovascular causes, 37 percent (95 percent confidence interval, 20 to 50 percent; P less than 0.001) for the development of severe heart failure, 22 percent (95 percent confidence interval, 4 to 37 percent; P = 0.019) for congestive heart failure requiring hospitalization, and 25 percent (95 percent confidence interval, 5 to 40 percent; P = 0.015) for recurrent myocardial infarction. CONCLUSIONS: In patients with asymptomatic left ventricular dysfunction after myocardial infarction, long-term administration of captopril was associated with an improvement in survival and reduced morbidity and mortality due to major cardiovascular events. These benefits were observed in patients who received thrombolytic therapy, aspirin, or beta-blockers, as well as those who did not, suggesting that treatment with captopril leads to additional improvement in outcome among selected survivors of myocardial infarction.

Adult↗
PubMed1992

Time to first pulse after automatic implantable cardioverter defibrillator implantation.

Should automatic implantable cardioverter defibrillator (AICD) power sources be explanted and discontinued if they have not pulsed during the first generator life? We have followed 59 patients an average of 23 months (range, 3 days to 8.4 years) after AICD implantation. The indication for AICD implantation was based on clinical dysrhythmia, history of sudden death, and findings at electrophysiologic study. Thirty-eight of 59 patients (64%) had experienced sudden death and 52/58 (90%) were inducible at electrophysiologic study. Excluding 5 inappropriate pulsing episodes, 31 of 59 patients (53%) had 235 pulses (range, 1 to 36; median, 2 pulses). The time to first pulse after implantation ranged from 1 day to 3.5 years with a median time of 2 months. In 6 patients, the first pulsing occurred later than 1 year after AICD implantation. Fifteen generators demonstrating impending power source failure have been replaced in 11 patients. Power source depletion occurred at an average of 24.1 months (range, 8 to 40 months). In 3 patients, the first pulsing occurred after generator depletion and replacement. By univariate analysis, none of 13 variables (sex, age, cardiac disease process, functional class, previous myocardial infarction, sudden death history, ejection fraction, type of dysrhythmia, inducibility with electrophysiologic testing, number of extra stimuli required for induction, left ventricular aneurysm resection, endocardial resection, or concomitant operation) was found to be a predictor of pulsing (p greater than 0.05). We conclude that the majority of patients with pulses after AICD implantation will have them during the first 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Antiarrhythmic drug therapy and cardiac mortality in atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators.

BACKGROUND AND OBJECTIVES: The relation between cardiac mortality and antiarrhythmic drug administration has not been fully determined. This relation was analyzed in 1,330 patients enrolled in the Stroke Prevention in Atrial Fibrillation Study, a randomized clinical trial comparing warfarin, aspirin and placebo for the prevention of ischemic stroke or systemic embolism in patients with nonvalvular atrial fibrillation. METHODS: Patients who received antiarrhythmic drug therapy for atrial fibrillation in this study were compared with patients not receiving antiarrhythmic agents. The relative risk of cardiac mortality, including arrhythmic death, in patients receiving antiarrhythmic drug therapy was determined and adjusted for other cardiac risk factors. RESULTS: In patients receiving antiarrhythmic drug therapy, cardiac mortality was increased 2.5-fold (p = 0.006, 95% confidence interval [CI] 1.3 to 4.9) and arrhythmic death was increased 2.6-fold (p = 0.02, 95% CI 1.2 to 5.6). Among patients with a history of congestive heart failure, those given antiarrhythmic medications had a relative risk of cardiac death of 4.7 (p less than 0.001, 95% CI 1.9 to 11.6) compared with that of patients not so treated; the relative risk of arrhythmic death in the treated group was 3.7 (p = 0.01, 95% CI 1.3 to 10.4). Patients without a history of congestive heart failure had no increased risk of cardiac mortality (relative risk 0.70, 95% CI 0.2 to 3.1) during antiarrhythmic drug therapy. After exclusion of 23 patients with documented ventricular arrhythmias and adjustment for other variables predictive of cardiac death, patients receiving antiarrhythmic drugs were not at increased risk of cardiac death or arrhythmic death. However, in patients with a history of heart failure who received antiarrhythmic drug therapy, the relative risk of cardiac death was 3.3 (p = 0.05, 95% CI 0.99 to 11.1) and that of arrhythmic death was 5.8 (p = 0.009, 95% CI 1.5 to 21.7) compared with the risk in patients not taking antiarrhythmic medications. CONCLUSIONS: Although antiarrhythmic drug therapy was not randomly determined in this trial, the data suggest that in patients with atrial fibrillation and a history of congestive heart failure, the risk of such therapy may outweigh the potential benefit of maintaining sinus rhythm.

Anti-Arrhythmia Agents↗
PubMed1992

Does dual chamber or atrial pacing prevent atrial fibrillation? The need for a randomized controlled trial.

Partially due to recent reports that cardiac antiarrhythmic therapy may have adverse effects on patient survival, clinicians have become more interested in the nonpharmacological prevention of atrial fibrillation. There is a large body of literature that suggests that the rate of development of atrial fibrillation in paced sick sinus syndrome patients is much lower in those patients who have received an atrial-based system, rather than a VVI system. However, all the published studies to date are retrospective, and fraught with potential bias favoring the AAI or DDD group. The authors strongly believe that the only way to determine if these suggestive but uncertain retrospective analyses are correct is to apply the same scientific rigor to this problem as has been applied to many other problems in cardiovascular medicine and perform a prospective randomized trial. A proposed trial design is discussed.

Atrial Fibrillation↗
PubMed1991

Early angioplasty in patients with acute myocardial infarction complicated by hypotension.

Emergency percutaneous transluminal coronary angioplasty was performed in 62 patients with acute myocardial infarction complicated by hypotension. All patients were treated within 12 hours of the onset of chest pain. Angioplasty was completely successful (residual lesion less than or equal to 50%) in 48 patients, partially successful (patent vessel greater than 50% residual lesion) in four patients, and unsuccessful in 10 patients. Patients in whom angioplasty was successful had a hospital mortality rate of 19%; those in whom angioplasty was unsuccessful or only partially successful had hospital mortality rates of 60% and 50%, respectively, (p = 0.012). Patients with occlusion of the proximal left anterior descending vessel had the highest failure rate (42%) and the highest mortality rate (67%). Other univariate predictors of hospital mortality were older age and elevated end-diastolic pressure. Successful emergency angioplasty improves mortality in patients with acute infarction complicated by hypotension.

Angioplasty, Balloon, Coronary↗
PubMed1990

Efficacy of betaxolol in the treatment of stable exertional angina pectoris: a dose-ranging study.

To assess the efficacy of oral betaxolol in the treatment of stable exertional angina pectoris and to determine the relationship between betaxolol doses/serum concentrations and clinical/hemodynamic responses the authors studied 24 patients prior to and following stepwise administration of 5, 10, 20, 40, and 80 mg doses. The major endpoint for the study was the achievement of clinical beta blockade (heart rate 50-60 beats/min and less than or equal to 20% rise in treadmill stage I heart rate). Betaxolol produced a decrease in mean angina pectoris frequency from 6.6 +/- 1.9 episodes/week with placebo to 0.2 +/- 0.5 episode/week during clinical beta blockade (p less than 0.00005). Mean treadmill exercise time increased from 3.1 +/- 1.7 min with placebo to 7.3 +/- 2.3 min with doses sufficient to reduce angina pectoris frequency greater than or equal to 75% (p less than 0.00005) and to 8.0 +/- 2.3 min during clinical beta blockade (p less than 0.00005). The mean doses of betaxolol required to produce a greater than or equal to 75% decrease in angina pectoris frequency and clinical beta blockade were 12 +/- 5 mg (range 5-40 mg) and 28 +/- 29 mg (range 5-80 mg) respectively. Mean serum concentrations associated with these clinical endpoints were 23.8 +/- 9.7 ng/mL and 59.7 +/- 54.0 ng/mL respectively. The results indicate that betaxolol, in widely ranging doses, is highly effective in reducing angina pectoris frequency and improving exercise capacity in patients with stable exertional angina pectoris.

Angina Pectoris↗
PubMed1989

Adverse effects of permanent cardiac internal defibrillator patches on external defibrillation.

At the time of left ventricular aneurysm resection, antiarrhythmic operations or other open-heart operative procedures in patients with ventricular dysrhythmia, permanent internal defibrillator patches may be inserted. Insertion of the energy source may be delayed due to its unavailability or to a desire for postoperative electrophysiologic study before its insertion. To assess the effects of permanent internal defibrillator patches on external defibrillation, 7 anesthetized calves were studied. Fibrillation-defibrillation studies were performed before and after insertion of permanent internal defibrillator patches (model L67, 27 cm2, Intec Systems), one on each ventricle. The values of percent successful defibrillation obtained before insertion of the patches, although much lower than values that would be expected in humans, are consistent with the results of an extensive earlier study involving this calf model. Similar values obtained after insertion of the patches are appreciably lower than the values obtained before implantation of the patches, and appreciably lower than the results predicted by the earlier study. A significant decrease in the percent of successful defibrillations (p less than 0.001) was observed for a shock intensity of approximately 400 J. Permanent internal cardiac defibrillator patches on the right and left ventricles reduce the probability of achieving successful defibrillation externally with unidirectional shocks. The wisdom of implanting permanent large internal cardiac defibrillator patches without the energy source is questioned.

Animals↗
PubMed1989

Emergency angioplasty in acute anterior myocardial infarction.

Ninety-three patients with acute anterior myocardial infarction were treated with emergency percutaneous transluminal coronary angioplasty (PTCA). All were found to have a high-grade obstruction in the left anterior descending (LAD) vessel or the bypass graft to this vessel; 64 patients had a total occlusion. A completely successful PTCA, defined as a residual lesion of less than or equal to 50%, was achieved in 73 (78%) patients. A partially successful PTCA, with a residual lesion of 51% to 99%, was achieved in 12 (13%) patients. PTCA was unsuccessful in eight (9%) patients. Hospital mortality was 14%. Three parameters viewed separately each predicted hospital mortality: presence of shock, a proximal location of the LAD vessel occlusion, and the residual stenosis after PTCA. Reocclusion was found in only 11% of patients but 34% had evidence of restenosis on restudy.

Aged↗
PubMed1989

Superiority of biphasic shocks in the defibrillation of dogs by epicardial patches and catheter electrodes.

Currently available internal cardiac defibrillators use a uniphasic, truncated exponential waveform morphology of about 6 msec in duration at an energy level of 23 to 33 joules. To determine if improved defibrillation could be achieved with a different waveform morphology, we implanted 4.5 cm2 titanium patches to the left and right ventricle of 28 dogs. After ventricular fibrillation was induced, defibrillation was attempted using 7, 12, 13, or 17 joules. A 5 msec rectangular uniphasic waveform morphology was compared with a 10 msec rectangular biphasic waveform with the lagging 5 msec pulse of half the amplitude of the leading 5 msec. In an additional seven dogs, a transvenous bipolar catheter was placed with the distal electrode in the right ventricular apex and the proximal electrode in the superior vena cava. Biphasic and uniphasic shocks were compared at 14 joules. In the patch-patch system, the biphasic waveform was superior to the uniphasic waveform at 7 joules (67% versus 35%, p less than 0.001) and at 12 joules (93% versus 78%, p less than 0.001). No statistically significant differences were achieved at 13 joules or 17 joules. In the catheter electrode system with a delivered energy of 14 joules, the biphasic waveform was more effective than the uniphasic waveform (87% versus 27%, p less than 0.001). Manufacturers of automatic implantable defibrillators should consider this information in the design of future automatic implantable defibrillators.

Animals↗