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Biomedical subjects

H R Middlekauff

Publications and source records attributed to H R Middlekauff.

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

Morning sympathetic nerve activity is not increased in humans. Implications for mechanisms underlying the circadian pattern of cardiac risk.

BACKGROUND: The sympathetic nervous system has been implicated in the circadian pattern of myocardial infarction and sudden death. It has been postulated that sympathetic nerve activity is higher in the morning than at other times of the day and that this increase reflects an endogenous circadian pattern or is triggered by changes in posture and the onset of morning activities. METHODS AND RESULTS: To test these two concepts, we made microneurographic recordings of muscle sympathetic nerve activity in the morning (6:30 to 8:30 AM) and afternoon (2:00 to 4:00 PM) in eight healthy subjects (mean age, 42 +/- 4 years), and intraindividual comparisons (paired t tests) were made during (1) supine rest, (2) postural changes simulated by lower body negative pressure (LBNP), and (3) activity produced by sustained handgrip. Plasma cortisol, known to follow a circadian pattern, was measured to assess whether normal circadian patterns were present under experimental conditions. Plasma cortisol exhibited a robust circadian variability (plasma cortisol [mean +/- SEM], AM versus PM: 17 +/- 1 versus 9 +/- 1 microgram/dL, P = .008). In contrast, basal muscle sympathetic nerve activity was not higher in the morning compared with the afternoon (group mean sympathetic nerve activity, AM versus PM: 38 +/- 6 versus 38 +/- 6 bursts per minute, P = NS). Similarly, plasma norepinephrine levels were not higher in the morning compared with the afternoon (plasma norepinephrine, AM versus PM: 157 +/- 17 versus 173 +/- 14 pg/mL, P = NS). During postural stress simulated by LBNP, the magnitude of change in sympathetic nerve activity was not higher in the morning compared with the afternoon (LBNP -20 mm Hg, AM versus PM: 103 +/- 34% versus 157 +/- 31%, P = NS). Finally, the magnitude of change in muscle sympathetic nerve activity during the first minute of handgrip exercise (AM versus PM: 11 +/- 17% versus 8 +/- 11%, P = NS) or the second minute of handgrip exercise (AM versus PM: 59 +/- 34% versus 60 +/- 15%, P = NS) was not higher in the morning compared with the afternoon. CONCLUSIONS: These findings challenge the concept that sympathetic nerve activity is higher in the morning either during supine rest or during postural changes and activity. We speculate that if the sympathetic nervous system is involved in the circadian pattern of sudden death, this involvement must reflect exaggerated morning end-organ responsiveness to norepinephrine, not enhanced morning sympathetic outflow.

Adult↗
PubMed1995

Antiarrhythmic prophylaxis vs warfarin anticoagulation to prevent thromboembolic events among patients with atrial fibrillation. A decision analysis.

BACKGROUND: Patients with atrial fibrillation compared with those with sinus rhythm are at increased risk for thromboembolism, often mandating therapy directed at thromboembolism prevention. However, the safest, most efficacious strategy to prevent thromboembolism associated with atrial fibrillation is unknown. We developed a decision analysis to compare the risks and benefits of two common clinical strategies to prevent thromboembolism in the patient with atrial fibrillation: (1) sinus rhythm maintenance with quinidine sulfate or with amiodarone hydrochloride after cardioversion and (2) long-term anticoagulation with warfarin sodium. METHODS: A search was conducted of the English-language MEDLINE databases of the National Library of Medicine dated 1966 through December 1992. The search was conducted by intersecting "quinidine," "warfarin," or "amiodarone" with "atrial fibrillation." Six of 249 articles concerning quinidine and five of 20 articles concerning warfarin were judged by multiple reviewers to meet predetermined inclusion and exclusion criteria. To our knowledge, no randomized, placebo-controlled trials of amiodarone therapy for atrial fibrillation have been published. Five of 112 identified articles concerning amiodarone involved nonrandomized trials that met the remaining selection criteria and were included in this analysis. RESULTS: Thromboembolic events and fatal nonthromboembolic adverse events during the course of therapy (defined as fatal proarrhythmia, fatal hemorrhage, and fatal noncardiac toxic effects) were considered to have equivalent weight. The total risk during therapy, defined as thromboembolic and fatal nonthromboembolic adverse events during the course of therapy, was evaluated over a range of baseline thromboembolism risks, from 1% to 20% per patient-year. Quinidine therapy compared with no therapy was associated with increased total risk, unless baseline thromboembolism risk exceeded 11% per patient-year. Total risk during warfarin therapy was less than total risk during quinidine therapy for the entire range of baseline thromboembolism risks, from 1% to 20% per patient-year. Total risk during warfarin or amiodarone therapy was similar and less than that with no therapy for the entire range of baseline risks. CONCLUSIONS: Based on data from randomized, controlled trials of quinidine and warfarin, warfarin therapy appears to be the safest strategy for thromboembolism prevention in the patient with atrial fibrillation. The role of low-dose amiodarone therapy appears promising and warrants further study in randomized, controlled trials.

Adolescent↗
PubMed1995

Risk of arterial embolization in 224 patients awaiting cardiac transplantation.

Of patients awaiting cardiac transplantation, 10% to 20% die before a donor heart becomes available. Embolization of left ventricular thrombus is a source of morbidity and mortality in this population. To define the incidence and possible risk factors for systemic arterial embolization, we examined the frequency of arterial embolic events and their relation to clinical, hemodynamic, and echocardiographic variables in 224 consecutive outpatients awaiting cardiac transplantation (left ventricular ejection fraction 0.20 +/- 0.07 and left ventricular end-diastolic dimension 76 +/- 11 mm). Over a follow-up period of 301 +/- 371 days, during which 82 (37%) patients received warfarin, arterial embolization occurred in 6 (3%) patients, 1 of whom was receiving and 5 of whom were not receiving warfarin (difference not specifically significant). The risk of embolization was not statistically different in patients with atrial fibrillation, previous embolization, or left ventricular thrombus on transthoracic echocardiogram, regardless of warfarin therapy. Cumulative risk of sudden death was similar for patients with or without echocardiographically documented left ventricular thrombus. Nonfatal bleeding complications associated with warfarin therapy occurred in 2 (2%) patients. Thus in patients who are awaiting cardiac transplantation and who receive anticoagulation therapy for left ventricular thrombus, atrial fibrillation, or previous arterial embolization, the incidence of clinically detectable arterial embolization is low despite severe ventricular dilatation. Embolization is not likely a major cause of sudden death or morbidity in this population.

Cardiomyopathy, Dilated↗
PubMed1995

Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars.

OBJECTIVES: This study sought to determine the relation of the paced QRS configuration and conduction delay during pace mapping to reentry circuit sites in patients with ventricular tachycardia late after myocardial infarction. BACKGROUND: The QRS configuration produced by ventricular pacing during sinus rhythm (pace mapping) can locate focal idiopathic ventricular tachycardias during catheter mapping, but postinfarction reentry circuits may be relatively large and contain regions of slow conduction. We hypothesized that for postinfarction ventricular tachycardia, 1) pacing during sinus rhythm at reentry circuit sites distant from the exit from the scar would produce a QRS configuration different from the tachycardia; and 2) a stimulus to QRS delay during pace mapping may be a useful guide to reentry circuit slow conduction zones. METHODS: Catheter mapping and ablation were performed in 18 consecutive patients with ventricular tachycardia after myocardial infarction. At 85 endocardial sites in 13 patients, 12-lead electrocardiograms (ECGs) were recorded during pace mapping, and participation of each site in a reentry circuit was then evaluated by entrainment techniques during induced ventricular tachycardia or by application of radiofrequency current. RESULTS: Pace maps resembled tachycardia at < 30% of likely reentry circuit sites identified by entrainment criteria and at only 1 (9%) of 11 sites where radiofrequency current terminated tachycardia. Analysis of the stimulus to QRS interval during entrainment with concealed fusion showed that the conduction time from the pacing site to the exit from the scar was longer at sites where the pace map did not resemble tachycardia. Evidence of slow conduction during pace mapping, with a stimulus to QRS interval > 40 ms was observed at > or = 70% of reentry circuit sites. CONCLUSIONS: At many sites in postinfarction ventricular reentry circuits, the QRS configuration during pace mapping does not resemble the ventricular tachycardia QRS complex, consistent with relatively large reentry circuits or regions of functional conduction block during ventricular tachycardia. A stimulus to QRS delay during pace mapping is consistent with slow conduction and may aid in targeting endocardial sites for further evaluation during tachycardia.

Aged↗
PubMed1994

Complex heart rate variability and serum norepinephrine levels in patients with advanced heart failure.

OBJECTIVES: This study was designed to examine the relation of the Poincaré plot heart rate variability pattern to sympathetic nervous system activity as assessed by serum norepinephrine. BACKGROUND: Poincaré plots demonstrate a complexity of beat to beat behavior not readily detected by other heart rate variability measures. Previous studies have described two abnormal Poincaré patterns in patients with heart failure: a torpedo pattern with reduced beat to beat variability and a complex pattern with clustering of points. METHODS: To assess the relation of these plots to sympathetic activity, plasma norepinephrine at rest and a standard deviation measure of heart rate variability were analyzed in 21 patients with heart failure (mean left ventricular ejection fraction [+/- SD] 0.22 +/- 0.05). RESULTS: Eleven subjects had a torpedo-shaped and 10 subjects had a complex Poincaré plot pattern. These two groups did not differ significantly in age, functional class, disease etiology, left ventricular ejection fraction, heart rate, ventricular ectopic activity or in a standard deviation measure of heart rate variability. However, patients with a complex Poincaré plot pattern had higher norepinephrine levels (722 +/- 373 pg/ml) than patients with torpedo-shaped plots (309 +/- 134 pg/ml) (p = 0.003). Patients with a complex pattern also had more severe hemodynamic decompensation, as evidenced by their higher levels of pulmonary capillary wedge and mean pulmonary artery pressures and lower values for cardiac index than those of patients with a torpedo-shaped plot. CONCLUSIONS: Complex Poincaré plots are associated with marked sympathetic activation and may provide additional prognostic information and insight into autonomic alterations and sudden cardiac death in patients with heart failure.

Electrocardiography, Ambulatory↗
PubMed1994

Independent control of skin and muscle sympathetic nerve activity in patients with heart failure.

BACKGROUND: Sympathetic excitation characterizes heart failure, but the underlying mechanisms remain unknown. Abnormal baroreflex restraint of sympathetic neural outflow has been proposed, since baroreflexes are known to be abnormal in heart failure. The purpose of this study was to determine if sympathetic activation in humans with heart failure is limited to regions governed by the baroreflexes or is generalized to other regions free from baroreflex control. METHODS AND RESULTS: We report the first direct recordings of skin sympathetic nerve activity (free from baroreflex control) in humans with heart failure and compare simultaneous skin and muscle (baroreflex-dependent) sympathetic peroneal nerve activity in six patients with severe heart failure (mean left ventricular ejection fraction, 0.19 +/- 0.06) and in six age-matched normal control subjects. Although muscle sympathetic nerve activity was markedly increased in heart failure patients (heart failure versus controls, 69 +/- 3 versus 21 +/- 2 bursts per minute; P < .001), skin sympathetic nerve activity was not increased (heart failure versus controls, 12 +/- 1 versus 15 +/- 1 bursts per minute; P = NS). CONCLUSIONS: The finding that skin sympathetic nerve activity in contrast to muscle sympathetic nerve activity is not increased in heart failure supports the concept that an altered reflex system, such as the baroreflexes, with nonuniform effects on muscle and skin sympathetic nerve activity, underlies sympatho-excitation in heart failure.

Adult↗
PubMed1993

Low-dose amiodarone for atrial fibrillation.

Concerns about proarrhythmia risk and inefficacy associated with class I antiarrhythmic drugs have revived interest in low-dose amiodarone (maintenance dose 200-400 mg/day) for suppression of atrial fibrillation. In nonrandomized trials of amiodarone for atrial fibrillation refractory to conventional agents, amiodarone has been successful in maintaining sinus rhythm in 53-79% of patients during a mean follow-up of 15-27 months. Intolerable side effects, including pulmonary toxicity, are in the range of 1-12% per year and resolve following amiodarone withdrawal in the majority of cases. Proarrhythmia risk associated with amiodarone, even in the setting of left ventricular dysfunction, is extremely low. In patients with congestive heart failure, in whom other pharmacologic options are limited by proarrhythmia risk and negative inotropism, preliminary experience with amiodarone is especially promising. Randomized trials are needed, directly comparing amiodarone to conventional antiarrhythmic therapy for atrial fibrillation suppression and comparing amiodarone to warfarin for thromboembolism prevention in patients with atrial fibrillation refractory to conventional antiarrhythmic drugs.

Amiodarone↗
PubMed1993

Transesophageal echocardiography during radiofrequency catheter ablation of ventricular tachycardia.

Radiofrequency lesion formation requires stable catheter tip/endocardial contact. Energy delivery is limited when temperatures are > 100 degrees C due to coagulum formation at the catheter tip. Transesophageal echocardiographic imaging may be useful for monitoring catheter position and detecting boiling. Transesophageal echocardiographic images were recorded during production of 22 radiofrequency lesions in bovine myocardium in a saline bath. Lesion size, tissue temperature and appearance of echo contrast (bubbles) were assessed. In 11 patients, transesophageal echocardiography was used to guide catheter movement and detect boiling during radiofrequency ablation for ventricular tachycardia. In the tissue bath, the appearance of echo bubbles was associated with visual bubbling at the catheter tip, tissue temperatures > 60 degrees C and larger lesions (284 +/- 165 vs 30 +/- 54 mm3; p < 0.001). In humans, transesophageal images easily identified the catheter tip in either ventricle and enabled continuous observation of electrode-tissue contact during radiofrequency application. Transesophageal echocardiographic bubbles appeared in 59 of 217 radiofrequency applications (27%). Continued radiofrequency application after appearance of bubbles was followed by an increase in impedance. Prolonged placement of the probe in heavily sedated patients resulted in a mild sore throat, but no other complications. Transesophageal echocardiographic imaging enables continuous monitoring of catheter position during radiofrequency energy application. The abrupt appearance of echo bubbles indicates boiling and impending coagulum formation at the catheter tip.

Adult↗
PubMed1993

Predicting death from progressive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Data were retrospectively reviewed on 528 consecutive patients hospitalized for treatment of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07) and cardiac transplant evaluation, who were stabilized with medical therapy and discharged home. Predictors of heart failure death or rehospitalization for urgent transplantation were identified using the Cox proportional-hazards model. Within 1 year, 59 patients (11%) died suddenly and 70 (13%) died of heart failure or required urgent transplantation. A serum sodium < or = 134 mEq/liter, pulmonary arterial diastolic pressure > 19 mm Hg, left ventricular diastolic dimension index > 44 mm/m2, peak oxygen consumption during exercise testing < 11 ml/kg/min and the presence of a permanent pacemaker were independent predictors of hemodynamic deterioration. In the absence of these risk factors the risk of hemodynamic deterioration within 1 year from this study was only 2%. This risk increased to > 50% in the presence of hyponatremia and any 2 additional risk factors. Thus, patients with advanced heart failure at highest risk for progressive hemodynamic deterioration can be identified from clinical variables that could aid in triaging such patients to earlier cardiac transplantation.

Actuarial Analysis↗
PubMed1993

Prognosis after syncope: impact of left ventricular function.

A cardiac cause of syncope has been associated with increased sudden death risk, whereas unexplained syncope has a benign prognosis. However, in patients who have depressed left ventricular function, the accuracy of diagnostic tests and the efficacy of therapy, such as antiarrhythmic drugs, are reduced. Previous studies of patients with syncope have not evaluated the contribution of left ventricular performance in risk stratification for sudden death. The purpose of our study of a large population of patients with syncope was to determine the impact of left ventricular dysfunction on sudden death risk if syncope is caused by a cardiac cause or remains unexplained after electrophysiologic testing. We retrospectively evaluated the relationship of left ventricular ejection fraction to sudden death prognosis in 88 consecutive patients referred for electrophysiologic testing to determine a cause of syncope. The mean age was 57 +/- 18 years, left ventricular ejection fraction was 0.41 +/- 0.20, and 66 patients (75%) had structural heart disease. In 49 patients (56%) a cardiac cause of syncope was diagnosed, and in 39 patients (44%) the cause of syncope remained unexplained after evaluation. Cardiac syncope was attributed to ventricular tachycardia in 27 patients, bradyarrhythmia in 11 patients, and supraventricular tachyarrhythmia in 11 patients. By logistic regression only structural heart disease was independently associated with cardiac cause of syncope (p = 0.003). After a mean follow-up of 790 +/- 688 days, nine patients had died suddenly, eight (89%) of whom had left ventricular ejection fraction less than 0.30.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Increased risk of progressive hemodynamic deterioration in advanced heart failure patients requiring permanent pacemakers.

To determine the influence of long-term permanent pacing systems on survival in patients with severe left ventricular dysfunction, data from 557 consecutive patients hospitalized with advanced heart failure for cardiac transplant evaluation and discharged on medical therapy were reviewed. Permanent pacemakers were identified in 42 (8%) patients. One-year actuarial risk of death from heart failure or urgent transplantation in paced patients was higher (49%) than that of a control group, matched for the severity of heart failure (15%, p = 0.003). Sudden death did not differ between paced patients and controls.

Actuarial Analysis↗
PubMed1993

Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope.

OBJECTIVES: The purpose of this study was to assess the importance of syncope as a warning sign for sudden death in advanced heart failure and to determine the relative importance of cardiac syncope and syncope from other causes. BACKGROUND: Despite remarkable advances in the pharmacologic approach to advanced heart failure, 20% to 40% of patients with advanced heart failure will die each year. In such patients, the relation between sudden death and the etiology of syncope has not been evaluated. METHODS: The relation of syncope to sudden death was evaluated in 491 consecutive patients with advanced heart failure (New York Heart Association functional class III or IV), no history of cardiac arrest and a mean left ventricular ejection fraction of 0.20 +/- 0.07. Patients were evaluated for the presence and origin of syncope. The severity of heart failure was assessed from serum sodium levels, ejection fraction, functional class and echocardiographic and hemodynamic variables. RESULTS: Sixty patients (12%) had a history of syncope; the condition had a cardiac origin in 29 (48%) and was due to other causes in 31 (52%). The origin of heart failure was coronary artery disease in 234 patients (48%) and dilated cardiomyopathy in 253 (51%) and its severity was similar in patients with and without syncope. During a mean follow-up interval of 365 +/- 419 days, 69 patients (14%) died suddenly and 66 patients (13%) died of progressive heart failure. The actuarial incidence of sudden death by 1 year was significantly greater in patients with (45%) than in those without (12%, p < 0.00001) syncope. In the Cox proportional hazards model, syncope predicted sudden death independent of atrial fibrillation, serum sodium, cardiac index, angiotensin-converting enzyme inhibition and patient age. The actuarial risk of sudden death by 1 year was similarly high in patients with either cardiac syncope or syncope from other causes (49% vs. 39%, p = NS). CONCLUSIONS: Patients with advanced heart failure are at especially high risk for sudden death regardless of the etiology of syncope.

Adult↗
PubMed1993

Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction.

BACKGROUND: Ventricular tachycardia reentry circuits in chronic infarct scars can contain slow conduction zones, which are difficult to distinguish from bystander areas adjacent to the circuit during catheter mapping. This study developed criteria for identifying reentry circuit sites using computer simulations. These criteria then were tested during catheter mapping in humans to predict sites at which radiofrequency current application terminated ventricular tachycardia. METHODS AND RESULTS: In computer simulations, effects of single stimuli and stimulus trains at sites in and adjacent to reentry circuits were analyzed. Entrainment with concealed fusion, defined as ventricular tachycardia entrainment with no change in QRS morphology, could occur during stimulation in reentry circuit common pathways and adjacent bystander sites. Pacing at reentry circuit common pathway sites, the stimulus to QRS (S-QRS) interval equals the electrogram to QRS interval (EG-QRS) during tachycardia. The postpacing interval from the last stimulus to the following electrogram equals the tachycardia cycle length. Pacing at bystander sites the S-QRS exceeds the EG-QRS interval when the conduction time from the bystander site to the circuit is short but may be less than or equal to the EG-QRS interval when the conduction time to the circuit is long. The postpacing interval, however, always exceeds the tachycardia cycle length. When conduction in the circuit slows during pacing, the S-QRS and postpacing intervals increase and the slowest stimulus train most closely reflects conduction times during tachycardia. Endocardial catheter mapping and radiofrequency ablation were performed during 31 monomorphic ventricular tachycardias in 15 patients with drug refractory ventricular tachycardia late after myocardial infarction. During ventricular tachycardia, trains of electrical stimuli or scanning single stimuli were evaluated before application of radiofrequency current at the same site. Radiofrequency current terminated ventricular tachycardia at 24 of 241 sites (10%) in 12 of 15 patients (80%). Ventricular tachycardia termination occurred more frequently at sites with entrainment with concealed fusion (odds ratio, 3.4; 95% confidence interval [CI], 1.4 to 8.3), a postpacing interval approximating the ventricular tachycardia cycle length (odds ratio, 4.6; 95% CI, 1.6 to 12.9) and an S-QRS interval during entrainment of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length (odds ratio, 4.9; 95% CI, 1.4 to 17.1). Ventricular tachycardia termination was also predicted by the presence of isolated diastolic potentials or continuous electrical activity (odds ratio, 5.2; 95% CI, 1.8 to 15.5), but these electrograms were infrequent (8% of all sites). Combinations of entrainment with concealed fusion, postpacing interval, S-QRS intervals, and isolated diastolic potentials or continuous electrical activity predicted a more than 35% incidence of ventricular tachycardia termination during radiofrequency current application versus a 4% incidence when none suggested that the site was in the reentry circuit. Analysis of the postpacing interval and S-QRS interval suggested that 25% of the sites with entrainment with concealed fusion were in bystander areas not within the reentry circuit. At restudy 5 to 7 days later, 6 patients had no monomorphic ventricular tachycardia inducible, and inducible ventricular tachycardias were modified in 4 patients. None of these 10 patients have suffered arrhythmia recurrences during a follow-up of 316 +/- 199 days, although 4 continue to receive previously ineffective medications. CONCLUSIONS: Regions giving rise to reentry after myocardial infarction are complex and can include bystander areas, slow conduction zones, and isthmuses for impulse propagation at which radiofrequency current lesions can interrupt reentry.

Aged↗
PubMed1992

Low-dose amiodarone for atrial fibrillation: time for a prospective study?

Because atrial fibrillation is associated with substantial morbidity, restoration of sinus rhythm is desirable. Long-term maintenance of sinus rhythm often requires chronic antiarrhythmic therapy. Class I antiarrhythmic drugs such as quinidine or propafenone maintain sinus rhythm in approximately 50% of patients at 1 year and have risks for proarrhythmia and noncardiac toxicity. Studies of low-dose amiodarone for atrial fibrillation have reported sinus rhythm maintenance in 53% to 79% of patients during a mean follow-up of 27 months. Amiodarone has a lower incidence of proarrhythmia and heart failure exacerbation compared with class I drugs. Most noncardiac side effects are dose related, and low-dose amiodarone (less than 300 mg/d) is well tolerated. The time has come for a large-scale prospective evaluation of low-dose amiodarone treatment early in the course of atrial fibrillation.

Amiodarone↗
PubMed1992

Prevention of sudden death in survivors of myocardial infarction: a decision analysis approach.

During the first year after myocardial infarction, 5% to 15% of patients die, and the majority of deaths occur suddenly. Highly efficacious therapy, such as the implantable cardioverter-defibrillator, may reduce the chance of sudden death, but broad application is limited by associated risks. Hence, attempts to identify patients at high risk so they can receive therapy are desirable. Subgroups with high or low sudden death risks can be identified based on left ventricular function. Further risk stratification using programmed electrical stimulation and the signal-averaged ECG has been advocated, but the best strategy is unknown. Using a decision analysis model, we compared the 1-year survival rates in survivors of myocardial infarction treated with the implantable cardioverter-defibrillator either empirically or based on screening with the signal-averaged ECG and programmed electrical stimulation. The best strategy for selecting patients for therapy depended on the pre-therapy sudden death risk. For patients at low risk, such as those with well-preserved ventricular function, antiarrhythmic therapy selected with screening tests or given empirically increased both the mortality rate resulting from the adverse effects of therapy and the excellent survival rate without therapy. In the moderate-risk population, both empiric and stratified approaches reduced mortality, but stratification substantially limited the number of patients receiving unnecessary therapy. In the high-risk population, empiric treatment achieved the best survival rate, and screening resulted in only a small reduction in the number of patients treated unnecessarily.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1992

Significance of aborted cardiac arrest and sustained ventricular tachycardia in patients referred for treatment therapy of advanced heart failure.

Cardiac arrest in patients with heart failure may be the result of remediable factors such as pulmonary edema, drug toxicity, or electrolyte abnormalities, or it may be due to primary arrhythmias. The relation of prior aborted cardiac arrest or sustained ventricular tachycardia to subsequent prognosis was assessed in 458 consecutive patients referred for management of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07). All patients received tailored vasodilator and diuretic therapy and were then followed as outpatients. Patients were divided into four groups: 388 patients (85%) with no prior cardiac arrest or sustained ventricular tachycardia, 31 patients (7%) with a primary arrhythmia cardiac arrest, 22 patients (5%) with a secondary cardiac arrest, and 17 patients (4%) with sustained ventricular tachycardia without cardiac arrest. Patients with cardiac arrest resulting from a primary arrhythmia were usually treated with antiarrhythmic drugs (25 patients), and five patients received an implantable defibrillator. After hospital discharge actuarial 1-year sudden death risk (17%) and total mortality (24%) rates for the group with primary arrhythmia were similar to corresponding values in patients with no history of cardiac arrest or sustained ventricular tachycardia (17% and 30%, respectively). In patients with a secondary cardiac arrest as a result of exacerbation of heart failure (11 patients), torsade de pointes (10 patients), or hypokalemia (one patient), therapy focused on removal of aggravating factors. Actuarial 1-year sudden death (39%) and total mortality (54%) rates for the group with secondary arrest were higher than for patients without a history of cardiac arrest (p = 0.003 and 0.005, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1992

Amiodarone therapy does not compromise subsequent heart transplantation.

OBJECTIVES: The objective of this study was to determine the frequency of pulmonary complications, feasibility of early hospital discharge and requirements for postoperative inotropic and chronotropic support in patients receiving amiodarone therapy before heart transplantation. BACKGROUND: Although many patients waiting for heart transplantation will die of arrhythmias before a donor heart is found, the use of amiodarone has been limited by concern about increased complications in the perioperative period. METHODS: The 29 patients receiving amiodarone at the time of heart transplantation at University of California, Los Angeles Medical Center between October 1986 and September 1990 were compared with 29 control recipients to evaluate postoperative morbidity. Patients were receiving amiodarone for recurrent ventricular tachyarrhythmias (n = 11), atrial fibrillation (n = 2) or complex ventricular ectopic activity (n = 16). The average daily dose was 360 +/- 230 mg/day for an average of 11 +/- 22 months before transplantation. Amiodarone and control groups had a similar ejection fraction (0.18 +/- 0.07 vs. 0.20 +/- 0.08), frequency of coronary disease, age and gender. There were three more status I patients in the control group. OKT3 was given to only two patients receiving amiodarone and 12 control patients at high risk for renal dysfunction. RESULTS: Postoperatively, the duration of assisted ventilation was 21 +/- 19 h after amiodarone therapy versus 26 +/- 2 h in the control group (20 +/- 18 h vs. 15 +/- 9 h after excluding patients receiving OKT3), discharge arterial oxygen saturation was > 95% in both groups. Two patients in the amiodarone group with a smoking history of > 100 pack-years developed bilateral pulmonary infiltrates of brief duration. Although patients receiving amiodarone required atrial pacing more frequently (eight vs. two patients) and had a lower heart rate at discharge (75 +/- 18 vs. 86 +/- 11 beats/min), the duration of inotropic support (2.1 +/- 1.5 vs. 3.5 +/- 2.5 days) and of hospital stay (10 +/- 3 vs. 15 +/- 10 days) was not higher in the amiodarone than in the control group. The mortality rate at 30 days was similar in the two groups (6.8% vs. 3.4%, p = NS). CONCLUSIONS: Amiodarone therapy before heart transplantation may contribute to occasional pulmonary complications but does not significantly increase perioperative morbidity or mortality with the regimens used in this retrospective study.

Aged↗