Max Weber

Clusters of ventricular tachycardias signify impaired survival in patients with idiopathic dilated cardiomyopathy and implantable cardioverter defibrillators.

OBJECTIVES This retrospective study was undertaken to provide data on occurrence, significance and therapy of ventricular tachyarrhythmia (VT) clusters (VTCs) in patients with dilated cardiomyopathy (DCM) and implantable cardioverter defibrillators (ICDs). BACKGROUND Data on the clinical significance of VTCs are lacking in patients with DCM and ICDs. METHODS Baseline characteristics of 106 consecutive patients with DCM and ICDs were prospectively collected, and chart reviews and episode data retrospectively analyzed. A VTC was defined as > or =3 sustained VTs/24 h. RESULTS During a mean follow-up of 33+/-23 months, 73 patients (68.9%) had recurrent VT or ventricular fibrillation (VF), 43 patients (40.6%) suffered only single VTs and 30 patients (28.3%) experienced 52 clusters of VTs. Actuarial survival free of VT or VF was 44.6%, 33.0% and 26.5%, and survival free of VTC was 77.3%, 72.2% and 67.1% after one, two and three years, respectively. Independent predictors of VT clusters were heart failure before ICD implantation (p = 0.033), presenting monomorphic VT (p = 0.044), EF <0.40 (p = 0.014) and inducible mVT, especially with right bundle branch block and superior axis configuration (p<0.001). Survival free of recurrent VTCs was 50.8%, 38.1% and 19.0% after one, two and three years, respectively. Once a VTC had occurred, only 56.7%, 46.4%, 30.9% and 15.5% of patients survived and were not transplanted after one, two, three and four years, respectively. Survival was even more reduced if a VTC was associated with cardiac decompensation: 65.6% and 21.9% after one and two years, respectively. CONCLUSIONS Despite antiarrhythmic intervention, clusters of VTs occur and recur frequently in patients with DCM. They signify impaired survival, especially if they are associated with cardiac decompensation, and may be a harbinger of progressive myocardial deterioration rather than a primarily arrhythmic problem. The benefit of ICD therapy may therefore be low in these patients.

Potential Benefit From Implantable Cardioverter-Defibrillator Therapy in Patients With and Without Heart Failure

BACKGROUND Whether patients with heart failure derive a benefit from therapy with implantable cardioverter-defibrillators (ICDs) has been questioned. The purpose of this study was to investigate whether New York Heart Association (NYHA) functional class had an impact on the potential benefit from ICD therapy as assessed from data stored in the memory of ICDs. METHODS AND RESULTS Between 1989 and 1996, 603 patients (77% men; 59% with coronary artery disease and 16% with dilated cardiomyopathy; age, 57+/-13 years; ejection fraction, 44+/-18%) were treated with an ICD with extended memory function (storage of electrograms and/or RR intervals from treated episodes) in combination with endocardial lead systems. The stages of heart failure (NYHA functional class I through III) at implantation were correlated with overall mortality and the recurrence of fast ventricular tachyarrhythmias (>240 bpm) during follow-up. The potential benefit of the device was estimated as the difference between overall mortality and the hypothetical death rate had the device not been implanted. The latter was based on the recurrence of fast and, without termination by the devices, presumably fatal ventricular tachyarrhythmias. In the overall group, a significant difference between hypothetical death rate and overall mortality was observed (13.9%, 23.5%, and 26.6% at 1, 3, and 5 years, respectively) that suggested a benefit from ICD implantation. In patients in NYHA class I, the estimated benefit, which increased over time, was 15.2%, 29.2%, and 35.6% after 1, 3, and 5 years, respectively. In patients in NYHA class II or III, the estimated benefit increased until the third year (21.8% and 21.9%, respectively) and then remained constant until the fifth year (22.9% and 23.8%, respectively). Even those patients in NYHA class III with a history of decompensated heart failure benefited from ICD implantation. CONCLUSIONS Analysis of stored ECG data suggests that in patients with a history of ventricular tachycardia or ventricular fibrillation, ICD therapy may lead to a prolongation of life in NYHA classes I through III. The initial benefit is greatest in patients in NYHA class II and class III, but the estimated benefit might persist longest for patients in NYHA class I.

Efficacy and Safety of the Initial Use of Stability and Onset Criteria in Implantable Cardioverter Defibrillators

Primary Programming of Stability and Onset Criteria. Introduction: Inappropriate therapies are the most frequent adverse event in patients with implantable cardioverter defibrillators (ICDs). Most ICDs offer a stability criterion to discriminate ventricular tachycardia (VT) from atrial fibrillation and an onset criterion to discriminate VT from sinus tachycardia. The efficacy and safety of these criteria, if used immediately after implantation, is unknown.

Syncope in patients with an implantable cardioverter-defibrillator: incidence, prediction and implications for driving restrictions

OBJECTIVES This retrospective study was undertaken to provide information on occurrence, risk prediction and prevention of syncope in patients with an implantable cardioverter-defibrillator (ICD). BACKGROUND ICDs effectively terminate ventricular tachycardia and fibrillation (VT/VF). Incapacitating symptoms, such as syncope, may still occur. METHODS We performed a retrospective analysis of data from 421 patients (clinical history, outpatient chart reviews and episode data) with mean (+/-SD) follow-up of 26 +/- 18 months. RESULTS Of 421 patients, 229 (54.4%) had recurrent VT/VF, and 62 (14.7%) had syncope. The actuarial survival rate free of VT/VF was 58%, 45% and 37% and that for survival free of syncope was 90%, 85% and 81% at 12, 24 and 36 months after implantation, respectively. Once VT/VF had occurred, 76%, 68% and 62% of patients remained free of syncope during the following 12, 24 and 36 months, and 68%, 64% and 56% remained free of second syncope 12, 24 and 36 months after first syncope, respectively. In cases of syncope, the mean cycle length (CL) of VT was 251 +/- 56 ms. A low baseline left ventricular ejection fraction (LVEF), induction of fast VT (CL <300 ms) during programmed ventricular stimulation and chronic atrial fibrillation (AF) were associated with an increased risk of syncope. If the LVEF was >40%, fast VT had not been induced, and patients had no chronic AF; 96%, 92% and 92% of patients remained free of syncope after 12, 24 and 36 months, respectively. Once patients had a VT recurrence, syncope during the first VT and a high VT rate were the strongest risk predictors of future syncope. CONCLUSIONS Identification of patients with an ICD with a low and high risk of syncope seems to be feasible and might help as a guide to driving restrictions in such patients.

Effect of ventricular fibrillation duration on the defibrillation threshold in humans.

GRADAUS, R., et al.: Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans. Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 ± 11 years, 19 coronary artery disease, NYHA 2.2 ± 0.4, left ventricular ejection fraction 0.42 ± 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 ± 3.6 J after 10.3 ± 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with ≤ 8 J. In these patients, the mean defibrillation threshold was 4.0 ± 2.1 J after 1.4 ± 0.3 seconds compared to 9.5 ± 3.1 J after 10.2 ± 1.1 seconds (P < 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs.

Akute thorakale Aortendissektion mit Verlegung der linken Koronararterie

ZusammenfassungDie akute thorakale Aortendissektion ist eine potentiell lebensbedrohliche Erkrankung, die eine rasche Diagnosestellung und Therapie erfordert. In dieser Kasuistik wird über eine 65jährige Patientin berichtet, bei der aufgrund einer ungewöhnlichen Befundkonstellation die Diagnose einer akuten thorakalen Aortendissektion erschwert wurde. Heftige Brustschmerzen und akrale Durchblutungsstörungen führten bei der bis dahin gesunden Patientin zur notfallmäßigen Klinikaufnahme. Die körperliche Untersuchung ergab eine Bradykardie von 40 Schlägen pro Minute, Zeichen einer Durchblutungsstörung der Akren ähnlich einer „Raynaud-Symptomatik” und eine Hypotonie mit 90/50 mm Hg. Das Aufnahme-Elektrokardiogramm zeigte bei bradykardem Sinusrhythmus eine T-Negativierung in V1 und eine geringe ST-Hebung (1 mV) in V3. Fünf Stunden später bot die Patientin eine selbstterminierende polymorphe, ventrikuläre Tachykardie und einen bifaszikulären Block mit einem Rechtsschenkelblock und einem linksanterioren Hemiblock. Unter der Annahme eines akuten Myokardinfarktes wurde eine Streptokinase-Lyse durchgeführt. Nach hämodynamischer Verschlechterung, Intubation und Beatmung erfolgte die Verlegung in unsere Klinik. Eine Koronarangiographie zeigte den Befund einer thorakalen Aortendissektion mit Verschluß der linken Koronararterie. Die Patientin verstarb noch im Katheterlabor.SummaryAortic dissection is the most common fatal condition that involves the aorta. Occasionally, symptoms mimick acute myocardial infarction leading to thrombolytic treatment. Accurate diagnosis in patients with chest pain is therefore essential. We describe a case of acute aortic dissection which resulted in myocardial infarction due to obstruction of the left coronary ostium. A 65-year-old female patient with no previous cardiac history was admitted to a local hospital because of severe chest pain of acute onset. Physical examination was normal except for a low blood pressure (90/50 mm Hg), heart rate 45 beats/min and parasthesia in both hands. The ECG showed sinus bradycardia with negative T-wave in V1 and with 1 mm ST-segment elevation in V3. A chest X-ray was normal. Five hours later, the patient experienced once more severe chest pain followed by nonsustained polymorphic ventricular tachycardia (Figure 1). Another ECG showed bifascicular bundle branch block (right bundle branch block and left anterior fascicular block). The ECG was interpreted as showing acute myocardial infarction and treatment with intravenous streptokinase started. Since the patient remained severely hypotensive despite infusion of dobutamine, she was intubated, ventilated and transferred to our hospital. Cardiac catheterization showed acute dissection of the ascending aorta with an aortic intimal flap and an occlusion of the left coronary artery (Figures 2a and b). During catheterization, she suffered a cardiac arrest from which she could not be resuscitated. A postmortem examination confirmed the acute aortic dissection which reached to the ostium of the left coronary artery (Figures 3a and b, 4a and b) and an anterior myocardial infarction probably due to intermitted diastolic obstruction of the ostium of the left coronary artery by an aortic intimal flap.Aortic dissection is the most common fatal condition that involves the aorta. Occasionally, symptoms mimic acute myocardial infarction leading to thrombolytic treatment. Accurate diagnosis in patients with chest pain is therefore essential. We describe a case of acute aortic dissection which resulted in myocardial infarction due to obstruction of the left coronary ostium. A 65-year-old female patient with no previous cardiac history was admitted to a local hospital because of severe chest pain of acute onset. Physical examination was normal except for a low blood pressure (90/50 mm Hg), heart rate 45 beats/min and parasthesia in both hands. The ECG showed sinus bradycardia with negative T-wave in VI and with 1 mm ST-segment elevation in V3. A chest X-ray was normal. Five hours later, the patient experienced once more severe chest pain followed by non-sustained polymorphic ventricular tachycardia (Figure 1). Another ECG showed bifascicular bundle branch block (right bundle branch block and left anterior fascicular block). The ECG was interpreted as showing acute myocardial infarction and treatment with intravenous streptokinase started. Since the patient remained severely hypotensive despite infusion of dobutamine, she was intubated, ventilated and transferred to our hospital. Cardiac catheterization showed acute dissection of the ascending aorta with an aortic intimal flap and an occlusion of the left coronary artery (Figures 2a and b). During catheterization, she suffered a cardiac arrest from which she could not be resuscitated. A postmortem examination confirmed the acute aortic dissection which reached to the ostium of the left coronary artery (Figures 3a and b, 4a and b) and an anterior myocardial infarction probably due to intermitted diastolic obstruction of the ostium of the left coronary artery by an aortic intimal flap.

Antitachycardia pacing for rapid VT during ICD charging: a method to prevent ICD shocks.

WEBER, M., et al.: Antitachycardia Pacing for Rapid VT During ICD Charging: A Method to Prevent ICD Shocks. In patients with ICDs, rapid VTs are usually treated with shocks. It is unknown, if antitachycardia pacing (ATP) delivered once for rapid VT during capacitor charging can avoid painful shocks without increasing the risk of syncope. In patients in whom rapid monomorphic VT (cycle length 300–220 ms) could be reproducibly induced during predischarge ICD testing, the success of cardioversion (defibrillation threshold plus 10 J) and a single ATP attempt (burst with 8 or 16 stimuli) was compared using a randomized crossover study design. Consciousness of the patients was checked by the signal from a button constantly pushed by the patient. In 20 patients (ejection fraction 0.50 ± 0.19) rapid VTs (253 ± 26 ms) were reproducibly induced. A single burst successfully terminated 11 (55%) of 20 rapid VTs, 6 episodes could not be terminated with a single burst pacing and 3 VTs accelerated. Rapid VTs not terminated by ATP were significantly faster than those that could be terminated (246 vs 258 ms, P = 0.026). Cardioversion (19 ± 3 J) terminated the VTs in all cases. No patient suffered syncope during rapid VTs. A single ATP may terminate rapid VT with cycle lengths < 300 ms in 55% of patients without increasing the risk of syncope. Therefore, in rapid VTs one attempt of ATP may be suitable as an additional therapy option during ICD capacitor charging to avoid painful shocks without compromise of safety. Thus, future ICDs should implement the option of ATP during charging of capacitors.

Follow-Up Techniques in Patients with Implantable Cardioverter/Defibrillators

Patients with implantable cardioverter/defibrillators (ICD) suffer frequent and various complications during follow-up1. Within a recent multicenter study including 820 patients with a third-generation ICD, 280 patients (34%) experienced adverse events within a follow-up of only 5 ± 5 months2. Thus, a close follow-up of these patients by a physician aware of typical complications should be warranted. The most common adverse event is inappropriate arrhythmia detection typically resolved by programming or drug changes3. Other adverse events which might be resolved by reprogramming are syncopes despite ICD therapy4, ventricular tachycardias below the programmed detection rate5, and painful cardioversion shocks delivered during haemodynamically tolerated ventricular tachycardias6. Further complications, such as infection of the ICD, lead dis-lodgements, insulation failures, lead perforation, and emboli from thrombi attached to the leads which might be detected during follow-up, frequently require surgical intervention1.