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Biomedical subjects

S H Hohnloser

Publications and source records attributed to S H Hohnloser.

At least 91 records · Page 5Linked to original sources
PubMed1997

T wave alternans during exercise and atrial pacing in humans.

INTRODUCTION: Evidence is accumulating that microvolt T wave alternans (TWA) is a marker of increased risk for ventricular tachyarrhythmias. Initially, atrial pacing was used to elevate heart rate and elicit TWA. More recently, a noninvasive approach has been developed that elevates heart rate using exercise. METHODS AND RESULTS: In 30 consecutive patients with a history of ventricular tachyarrhythmias, the spectral method was used to detect TWA during both atrial pacing and submaximal exercise testing. The concordance rate for the presence or absence of TWA using the two measurement methods was 84%. There was a patient-specific heart rate threshold for the detection of TWA that averaged 100 +/- 14 beats/min during exercise compared with 97 +/- 9 beats/min during right atrial pacing (P = NS). Beyond this threshold, there was a significant and comparable increase in level of TWA with decreasing pacing cycle length and increasing exercise heart rates. CONCLUSIONS: The present study is the first to demonstrate that microvolt TWA can be assessed reliably and noninvasively during exercise stress. There is a patient-specific heart rate threshold beyond which TWA continues to increase with increasing heart rates. Heart rate thresholds for the onset of TWA measured during atrial pacing and exercise stress were comparable, indicating that heart rate alone appears to be the main factor of determining the onset of TWA during submaximal exercise stress.

Adult↗
PubMed1997

Electrophysiologic features of torsades de pointes: insights from a new isolated rabbit heart model.

INTRODUCTION: The exact electrophysiologic mechanism of torsades de pointes (TdP) is under intense investigation. No isolated animal heart model of this particular arrhythmia exists. METHODS AND RESULTS: In isolated rabbit hearts, TdP was induced by means of bradycardia in the presence of a high concentration of d-sotalol (10(-4) M) and shortly after lowering the concentration of potassium and magnesium in the perfusate. Multiple simultaneous epicardial and endocardial monophasic action potentials (MAPs) and volume-conducted 12-lead ECGs were recorded. d-Sotalol prolonged repolarization and increased dispersion of ventricular repolarization compared to baseline recordings. With the onset of low potassium and magnesium concentrations, repolarization was further prolonged and dispersion of repolarization was further increased followed by the occurrence of early afterdepolarizations (EADs) in the majority of MAP recordings, i.e., at both endocardial and epicardial locations of both ventricles. Upon increase of EAD amplitude, triggered arrhythmias with TdP of up to 42 beats ensued in 10 of 11 hearts studied. MAP duration at 90% repolarization (APD90), dispersion of APD90, and the incidence of EADs as well as dispersion of the QT interval and T wave area were significantly higher in beats triggering bigemini, couplets, or runs of TdP. CONCLUSION: TdP observed in this new isolated heart model was associated with markedly increased dispersion of ventricular repolarization and the occurrence of EADs in multiple locations of the heart. TdP is initiated when the amplitude of an EAD reaches threshold for initiation of the first beat of an episode.

Action Potentials↗
PubMed1997

Differential effects of D-sotalol, quinidine, and amiodarone on dispersion of ventricular repolarization in the isolated rabbit heart.

INTRODUCTION: Increased dispersion of ventricular repolarization has been suggested as a cause of proarrhythmic effects of Class IA or III antiarrhythmic drugs, such as d-sotalol, quinidine, and amiodarone. METHODS AND RESULTS: The influence of d-sotalol, quinidine, and amiodarone on the dispersion of monophasic action potential (MAP) durations was studied in 55 isolated Langendorff-perfused rabbit hearts at different pacing cycle lengths (CLs). MAP duration measured at 90% repolarization (APD90) was determined from 6 to 8 endocardial and epicardial MAP recordings with dispersion of ventricular repolarization defined as the range of APD90. The protocol was repeated 60 minutes after initiation of a perfusate containing increasing concentrations of d-sotalol (n = 12, 10[-6] M, 10[-5] M, and 5 x 10[-5] M) and quinidine (n = 8, 10[-6] M and 10[-5] M). Seventeen rabbits were fed with an aqueous solution of amiodarone (50 mg/kg per day over 4 weeks). The data of these experiments (n = 17) were compared with a series of 18 untreated control rabbits. Dispersion of ventricular repolarization was unchanged with the low concentration of d-sotalol (10[-6] M) but was increased-particularly at long CLs-with higher d-sotalol concentrations. With both concentrations of quinidine, dispersion of ventricular repolarization was increased in a rate-independent manner. Amiodarone did not affect dispersion of ventricular repolarization. CONCLUSIONS: Rate-dependent and concentration-dependent increases in dispersion of ventricular repolarization by d-sotalol and quinidine in this isolated rabbit heart model may help explain their proarrhythmic effects while the absence of an increase in dispersion of ventricular repolarization with amiodarone correlates with its clinically observed lower incidence of proarrhythmia.

Action Potentials↗
PubMed1996

Patency of infarct-related artery. Effect of restoration of anterograde flow on vagal reflexes. ATRAMI (Automatic Tone and Reflexes After Myocardial Infarction) Investigators.

BACKGROUND: In post-myocardial infarction (MI) patients, the restoration of anterograde flow in the infarct-related artery (IRA) significantly improves survival. Limitation of infarct size and increased electrical stability of the myocardium are likely operating mechanisms for this beneficial effect. We tested the hypothesis that patency of the IRA may enhance vagal reflexes, a factor known to affect electrical stability of the infarcted myocardium. METHODS AND RESULTS: Analysis of angiographic data was performed in 359 of 1284 post-MI patients enrolled in a multicenter prospective study within 8 weeks after the index MI. All the patients underwent baroreflex sensitivity (BRS) assessment by the phenylephrine method. The BRS of the entire population averaged 8.2+/-5.5 ms/mm Hg and was significantly related to age but not to ejection fraction (EF). One-, two-, and three-vessel disease was present in 138, 96, and 99 patients, respectively, while no coronary stenosis was observed in 26. IRA patency was documented in 234 patients (65%), while in the remaining 125 (35%), the artery remained occluded. Patients with occluded IRAs had more extensive coronary disease (2 to 3 vessels, 71% versus 46%, P<.01) and more depressed left ventricular (LV) function (LVEF, 48+/-13% versus 53+/-12%, P<.001). Patency of the IRA was associated with higher BRS values (BRS, 8.9+/-5.8 versus 7.1+/-4.7 ms/mm Hg, P<.005) and with a lower incidence (9% versus 18% P<.02) of markedly depressed BRS (<3 ms/mm Hg), a condition suggested by preliminary studies to be associated with an increased risk of post-MI mortality. The association between IRA patency and BRS was more evident in anterior than in inferior MI. Multivariate regression analysis showed that age of the patient and patency of the IRA were the major independent determinants of BRS, while LVEF was weakly related to BRS and only when analyzed as a categorized variable. CONCLUSIONS: The presence of an open IRA is associated with higher baroreflex sensitivity, and this effect is largely independent of limitation of infarct size by IRA patency. These data offer new insights into the mechanisms by which coronary artery patency may affect cardiac electrical stability and survival.

Adult↗
PubMed1996

Prospective comparison of flecainide versus quinidine for the treatment of paroxysmal atrial fibrillation/flutter. The Flecainide Multicenter Atrial Fibrillation Study Group.

In order to compare the efficacy and long-term tolerability of flecainide acetate versus quinidine, 239 patients with paroxysmal atrial fibrillation were prospectively treated with flecainide (n = 122) or quinidine (n = 117) in an open-label, randomized trial. All patients were followed for 1 year after initiation of therapy unless their antiarrhythmic drug was discontinued due to an inadequate therapeutic response or intolerable side effects. Although both drugs were equally effective in adequately controlling recurrences of atrial fibrillation (difference, p = 0.282; not significant), fewer flecainide patients had to have their therapy discontinued due to adverse experiences (p = 0.012). Based on both endpoints (efficacy and tolerability), an estimated 70.5% of flecainide versus 55.4% of quinidine patients would remain effectively treated at the end of 1 year on therapy (p < or = 0.007). The findings of this prospective study suggest that in the treatment of paroxysmal atrial fibrillation (1) flecainide and quinidine are equally effective in the acceptable suppression of symptomatic paroxysmal atrial fibrillation; (2) flecainide is better tolerated than quinidine and is less likely to be discontinued due to adverse effects; and (3) given the overall endpoint of efficacy and tolerability, more patients are likely to continue long-term therapy with flecainide than with quinidine.

Administration, Oral↗
PubMed1996

A randomized comparison of flecainide versus verapamil in paroxysmal supraventricular tachycardia. The Flecainide Multicenter Investigators Group.

Reentrant paroxysmal supraventricular tachycardia (PSVT) are frequently encountered in clinical practice. Verapamil and flecainide have both been successfully used as chronic oral therapy to prevent PSVT recurrences. This open-label, randomized, multicenter study was designed to compare the efficacy and adverse effects of verapamil (median dose, 240 mg/day) versus flecainide (median dose, 200 mg/day) in patients with frequent and symptomatic attacks of PSVT (other than atrial fibrillation or flutter). A total of 121 patients receiving flecainide (n = 63) or verapamil (n = 58) were followed for 8.1 +/- 5.1 and 7.5 +/- 5.4 months, respectively. Response was judged clinically as effective or not by the treating physician. By life table analysis, 11% discontinued flecainide and 19% discontinued verapamil for inefficacy at 1 year (difference not significant). Both groups showed a marked reduction in the frequency of attacks of PSVT. Before therapy, 71% of flecainide patients and 73% of verapamil patients had > or = 2 attacks per month. During therapy, 86% of all flecainide patient-months and 73% of all verapamil patient-months occurred with 0 or 1 attack; 19 (30%) patients on flecainide completed the trial ( > 270 days) without symptomatic attacks versus 7 (13%) of the patients on verapamil (p = 0.026). Both drugs were well tolerated; 19% of the flecainide group discontinued primarily because of adverse effects, compared with 24% discontinuing verapamil for this reason (difference not significant). Both flecainide and verapamil are effective and well tolerated for the prevention of recurrences of PSVT. For patients in whom radiofrequency ablation procedures cannot be performed or are not indicated, either therapy is a reasonable choice for long-term prophylaxis.

Administration, Oral↗
PubMed1996

Implantable cardioverter defibrillator therapy in a patient with the idiopathic long QT syndrome.

The idiopathic long QT syndrome (LQTS) carries a high mortality in untreated patients. Administration of beta-receptor antagonists is considered the treatment of choice. Data concerning the usefulness of implantable cardioverter-defibrillator (ICD) therapy in this condition are sparse. We report on a 29-year-old female with LQTS who was treated with propranolol, but also underwent implantation of an ICD as a fail-safe therapy. During the next 17 months, the patient was asymptomatic. However, after skipping her propranolol for 3 days, she had several syncopal spells with concomitant device therapy. ICD interrogation revealed a total of 55 nonsustained runs of ventricular tachycardia and 16 sustained episodes that were correctly identified by the device and respectively terminated by the first shock. This case report demonstrates that in selected patients with the LQTS, using ICD therapy as a fail-safe treatment may be life-saving, particularly when compliance to medical therapy is uncertain.

Adult↗
PubMed1996

Radiofrequency catheter ablation of atrial flutter after orthotopic heart transplantation.

INTRODUCTION: Antiarrhythmic drug refractory recurrent atrial flutter occurred in a 39-year-old man who had undergone successful orthotopic heart transplantation 3 months ago. METHODS AND RESULTS: At electrophysiologic study, the transplanted right atrium showed type I atrial flutter. The recipient right atrium was in sinus rhythm with complete atrioatrial dissociation of electrical activity. Mapping demonstrated double-spike electrograms in the low posterior region of the donor right atrium. During radiofrequency current application near this site, the double potentials were dissociated progressively and atrial flutter was terminated immediately. Thereafter, both the recipient and the transplanted atria were in sinus rhythm of different cycle lengths with continued electrical dissociation. CONCLUSION: This is the first report of successful radiofrequency catheter ablation of atrial flutter in a transplanted heart. Although mapping of the arrhythmia is more difficult due to the large circumference of the right atrium, which consists of parts of the recipient right atrium and the transplanted atrium, ablation should be considered in those patients with drug refractory supraventricular tachyarrhythmias.

Adult↗
PubMed1996

Changes in plasma epinephrine concentration and in heart rate during head-up tilt testing in patients with neurocardiogenic syncope: correlation with successful therapy with beta-receptor antagonists.

INTRODUCTION: Tilt table testing is widely used in the management of patients with neurocardiogenic syncope. However, the exact pathophysiologic mechanism of this disorder is still under debate. Likewise, therapy of these patients continues to represent a challenge in many cases. Therefore, the present study aimed to gain further insight into the pathophysiology of this syndrome and to examine easily accessible clinical parameters that can improve therapy selection. METHODS AND RESULTS: In 16 patients with neurocardiogenic syncope, changes in endogenous catecholamine concentrations were determined during repeated tilt table testing before and during treatment with metoprolol. Tachycardia preceded syncope in 8 of 10 responders compared to only 1 of 6 nonresponders (P < 0.05). In responders, the relative increase in epinephrine levels averaged 197% +/- 51% during drug-free tilting and 75% +/- 33% during repeated testing while on beta-blocker therapy (P < 0.05). In nonresponders, there was a smaller relative increase in epinephrine averaging 137% +/- 35% at baseline tilt. During repeated tilt testing, a similar increase was observed in these patients with recurrent syncope (156% +/- 104%; P = NS compared to baseline). CONCLUSION: In patients with neurocardiogenic syncope who show both an increase in epinephrine concentration during tilt test and sinus tachycardia prior to the onset of symptoms, beta-blocker treatment is very effective. These findings confirm the major role of sympathetic activation as a trigger of syncope. Particularly, heart rate changes at the onset of syncope may allow early identification of patients responding to antiadrenergic therapy.

Adrenergic beta-Antagonists↗
PubMed1996

[Stratification of patients at risk for sudden cardiac death with special reference to the autonomic nervous system].

The autonomic nervous system plays a decisive role in the genesis of sudden cardiac death. During recent years, two noninvasive tests for quantitative assessment of cardiac autonomic tone have become available: analysis of heart rate variability from 24-h ambulatory recordings and determination of baroreflex-sensitivity by means of the phenylephrine method. Numerous experimental and clinical studies suggest that heart rate variability assesses tonic vagal activity whereas baroreflex-sensitivity is considered to reflect phasic or reflex vagal activity. Both methods, however, are not redundant but rather complimentary. An advantage of assessment of baroreflex-sensitivity is represented by the fact that it can be performed under controlled laboratory conditions which yields a good intra- and interindividual comparability of test results. Some retrospective as well as prospective studies have assessed the value of determination of cardiac autonomic tone with respect to risk stratification after myocardial infarction. In general, these studies indicate that the combined assessment of autonomic tone together with left ventricular function yields an improved prediction particularly of the risk of dying due to arrhythmic events. It appears that baroreflex-sensitivity is particularly useful to predict arrhythmic events whereas heart rate variability seems to be linked more to cardiovascular mortality. Preliminary results of the largest prospective study of this kind, the ATRAMI study, indicate that the combined assessment of LVEF and baroreflex-sensitivity considerably improve risk stratification after myocardial infarction. If the final analysis of this trial confirms this, prospective interventional studies should be initiated to evaluate our ability of reducing the risk of sudden death based on noninvasive risk stratification.

Animals↗
PubMed1995

Efficacy and safety of d-sotalol, a pure class III antiarrhythmic compound, in patients with symptomatic complex ventricular ectopy. Results of a multicenter, randomized, double-blind, placebo-controlled dose-finding study. The d-Sotalol PVC Study Group.

BACKGROUND: There is increasing interest in pure class III antiarrhythmic compounds, ie, drugs in which the electrophysiological effect is confined to the propensity for producing an isolated lengthening of action potential duration. d-Sotalol represents the prototype of such pure class III agents. This double-blind, placebo-controlled, randomized dose-finding study evaluated the antiarrhythmic efficacy and safety of d-sotalol in patients with symptomatic chronic ventricular ectopy. METHODS AND RESULTS: A total of 233 patients presenting with > or = 30 premature ventricular contractions (PVCs) per hour during drug-free Holter monitoring randomly received placebo or d-sotalol at dosages of 50, 100, or 200 mg BID. Drug efficacy was assessed by repeat Holter monitoring at the end of double-blind therapy. There was a dose-dependent increase in QT and QTc duration, indicating class III activity. A dose-related decrease in hourly PVC counts was observed, reaching statistical significance for patients receiving 200 mg d-sotalol BID (311 PVCs/h during baseline compared with 135 PVCs/h during active treatment, P < .05). Analysis of the primary efficacy criterion (ie, > or = 75% reduction in total PVCs/h) revealed a significant treatment effect only for the highest d-sotalol dose, with 8 patients (14%) meeting this criterion. Eighteen patients reported side effects, which led to drug discontinuation in 5. One sudden death and one nonfatal cardiac arrest occurred in patients with dilative cardiomyopathy receiving 200 mg d-sotalol BID. No incidence of torsade de pointes was reported. CONCLUSIONS: d-Sotalol exerts dose-dependent class III activity in patients with symptomatic ventricular ectopy. Its PVC-suppressing activity is modest and becomes evident predominantly at dosages of 200 mg administered BID. The observation of drug-associated serious adverse arrhythmic events emphasizes the need for individualized careful dose titration, particularly in patients with advanced organic heart disease.

Adolescent↗
PubMed1995

Assessment of acute myocardial necrosis after cardiopulmonary resuscitation and cardioversion by means of combined thallium-201/technetium-99m pyrophosphate tomography.

Diagnosis of acute myocardial necrosis by means of conventional electrocardiographic criteria or the release of cardiac enzymes is often difficult or even impossible in patients with out-of-hospital cardiac arrest due to ventricular fibrillation with subsequent cardiopulmonary resuscitation including several DC countershocks. Simultaneous thallium-201/technetium-99m pyrophosphate (PYP) tomography was prospectively applied to 57 patients without typical clinical or electrocardiographic signs of acute myocardial infarction within 48 h after successful resuscitation from out-of-hospital cardiac arrest. Scintigraphic evidence of acute necrosis was present in 23/57 patients (40%). Increased 99mTc-PYP uptake in the pericardial tissue was found in 24 patients (42%). Maximal creatine kinase (CK) concentration was increased in 50/57 patients (88%). CK-MB activity averaged 68+/-52 U/l in patients with positive and 17+/-13 U/l in patients with negative tomograms (P<0.0005), demonstrating the validity of 201Tl/99mTc-PYP tomography. It may be concluded that simultaneous 201Tl/99mTc-PYP tomography is a valuable tool for evaluation of myocardial necrosis after cardiopulmonary resuscitation including DC countershock. Acute myocardial necrosis, as indicated by scintigraphy, represents a potential trigger for the occurrence of ventricular fibrillation. Therefore, 201Tl/99mTc-PYP tomography can be recommended in order to guide further diagnostic and therapeutic interventions in patients after cardiopulmonary resuscitation in whom the underlying cause of the occurrence of ventricular fibrillation is obscure.

Acute Disease↗
PubMed1995

Efficacy and proarrhythmic hazards of pharmacologic cardioversion of atrial fibrillation: prospective comparison of sotalol versus quinidine.

OBJECTIVES: This study compared the efficacy and safety of sotalol and quinidine for conversion and prevention of recurrent atrial fibrillation. BACKGROUND: Atrial fibrillation is the most common arrhythmia. Pharmacologic therapy has been advocated for both immediate restoration of sinus rhythm and prevention of recurrent atrial fibrillation. Quinidine is the therapeutic mainstay for both purposes, but its safety has recently been questioned. Although sotalol has been used successfully to maintain sinus rhythm after direct current cardioversion, its efficacy in pharmacologically reverting atrial fibrillation has not been examined. METHODS: Fifty consecutive patients with persistent atrial fibrillation were randomized to receive quinidine or sotalol for up to 7 days to restore sinus rhythm. Patients were followed up for 6 months. RESULTS: Quinidine was more effective than sotalol in terminating atrial fibrillation (60% vs. 20%, p = 0.009). When nonresponders to drug therapy underwent subsequent direct current cardioversion, total conversion rates in the quinidine and sotalol groups were comparable (88% vs. 68%, p = 0.17), as was the efficacy of the two drugs in preventing recurrent atrial fibrillation. Side effects necessitating drug discontinuation were more often observed with quinidine. No patient receiving sotalol but four patients receiving quinidine had drug-associated arrhythmia (torsade de pointes in three patients, sustained ventricular tachycardia in one patient). Precordial QT dispersion determined on the surface electrocardiogram (ECG) increased with quinidine (mean +/- SD 34 +/- 9 vs. 44 +/- 16 ms, p = 0.02), indicating enhanced inhomogeneity in ventricular repolarization. There was no change in QT dispersion in patients receiving sotalol (36 +/- 18 vs. 40 +/- 17 ms, p = 0.44). CONCLUSIONS: Quinidine is more effective than sotalol in terminating atrial fibrillation but is associated with more side effects. The proarrhythmic risk may be related to quinidine's propensity to increase disparity in ventricular repolarization. This risk warrants careful ECG monitoring during the 1st 4 to 7 days of therapy. Because most proarrhythmic effects occurred shortly after restoration of sinus rhythm, observation should continue > or = 2 to 3 days after sinus rhythm is reestablished.

Aged↗
PubMed1995

Proarrhythmia with class III antiarrhythmic drugs: definition, electrophysiologic mechanisms, incidence, predisposing factors, and clinical implications.

Antiarrhythmic drugs can and do induce unexpected and sometimes fatal reactions by either producing new symptomatic arrhythmias or by aggravating existing arrhythmias. The definition of proarrhythmia has changed since controlled clinical studies showed a dichotomy between arrhythmia suppression and mortality. The nature of proarrhythmic reactions is linked to the electrophysiologic effects of various antiarrhythmic drugs. Whereas Class I agents without accompanying effects on repolarization generally produce ventricular tachycardia (often incessant) or fibrillation, Class III agents typically produce torsades de pointes that may deteriorate into ventricular fibrillation. The precise mechanism of torsades de pointes is not fully elucidated, although early after-depolarization and increases in spatial or temporal dispersion of repolarization are likely possibilities. Proarrhythmic risk is lowest for amiodarone and is probably related to the drug's complex electrophysiologic profile. The incidence of torsades with sotalol increases with dose and the baseline values of the QT interval; the incidence with d-sotalol and other pure Class III agents remains unclear. Prospective, randomized, placebo-controlled studies to evaluate this are under way. The fact that d-sotalol increases mortality in postinfarction patients suggests that it may possibly be a common property of most, if not all, pure Class III compounds. The ongoing clinical trials with various Class III agents are likely to provide the critical information on this important therapeutic issue.

Amiodarone↗
PubMed1995

Circadian variation of heart rate variability in postinfarction patients with and without life-threatening ventricular tachyarrhythmias.

INTRODUCTION: Determination of heart rate variability (HRV) is widely used for noninvasive assessment of cardiac autonomic tone. A decreased HRV is associated with an increased mortality in patients surviving an acute myocardial infarction. There are, however, only sparse data about the circadian variation of different components of HRV that may be linked to the well-known circadian fluctuations in the occurrence of sudden death. In addition, the potential prognostic impact of circadian variations of HRV has not been examined. METHODS AND RESULTS: The present study compared the circadian variation of HRV from 14 postinfarction patients who had survived at least one episode of out-of-hospital cardiac arrest (cardiac arrest group) with that of 14 age- and sex-matched patients without a history of malignant arrhythmias after their index infarct (control group). Several time- and frequency-domain measures of HRV were assessed from 24-hour Holter recordings. Circadian variations of high- (HF), low- (LF), and total-frequency (TF) components were determined by calculating for each parameter the hourly difference from the day's mean. The average of these differences was calculated for every hour as well as for predefined day and night periods. There was no significant difference between the two groups with regard to HRV indices that predominantly reflect vagal tone, such as SDNN (78 +/- 25 vs 96 +/- 24 msec), pNN50 (2.7% +/- 4.6% vs 4.9% +/- 4.2%), or HF (6.3 +/- 3.0 vs 7.8 +/- 3.2 msec; cardiac arrest vs control group). There was also no significant difference in the circadian variation of LF or TF between the two groups during daytime and nighttime. However, a significant difference in circadian variation of HF was found during daytime (0.02 +/- 0.5 vs -0.6 +/- 0.5 msec; P = 0.006) and nighttime (0.19 +/- 0.64 vs 1.5 +/- 0.75 msec; P = 0.0002). In cardiac arrest survivors, there was no difference in the mean deviation of HF between the day- and the nighttime periods. CONCLUSIONS: These results show an almost complete abolition in circadian variation of parasympathetic tone in postinfarction patients surviving an episode of out-of-hospital cardiac arrest, whereas circadian variation of sympathetic tone is comparable to that of postinfarction patients without arrhythmic episodes. These findings indicate that determination of diurnal variation of HRV may add to the prognostic value of HRV with respect to identifying patients at high risk of sudden death.

Autonomic Nervous System↗