Arrhythmic risk stratification of post-myocardial infarction patients.

Post-myocardial infarction risk stratification, especially arrhythmic risk stratification, is an issue that has still not been wholly addressed in modern clinical cardiology. In the past 10 years, arrhythmic risk stratification has been approached mainly by evaluating frequency and complexity of premature ventricular contractions, detected on Holter monitoring, often in association with determination of percent ejection fraction. This methodology has been proven to be limited and fallacious according to the Cardiac Arrhythmia Suppression Trial I and II (CAST I,II) results, in which suppression of premature ventricular contractions or premature ventricular beats throughout by antiarrhythmic drugs resulted in an increase in both cardiac and arrhythmic mortality. Only amiodarone as an antiarrhythmic drug, as proven in the recent European Myocardial Infarct Amiodarone Trial (EMIAT) and Canadian Amiodarone Myocardial Infarction Trial (CAMIAT), was effective in reducing arrhythmic mortality without affecting cardiac mortality, in patients selected mainly because of a reduced ejection fraction, with and without premature ventricular contractions. Conversely, it is well known that beta-blockers are effective in preventing sudden death in post-acute myocardial infarction (AMI) patients, thus reducing cardiac and arrhythmic mortality. Conversely, in other institutions, risk stratification in post-AMI patients has been performed by electrophysiologic study obtained, without any previous noninvasive arrhythmic risk stratification, in all post-AMI patients. In recent years, many other noninvasive electrocardiology parameters, such as late potentials (signal-averaged electrocardiography), heart rate variability, baroreflex sensitivity, and, more recently, T-wave alternance, have been shown to be useful, but they are associated with a low specificity in the noninvasive identification of patients at high risk for arrhythmic mortality. Conversely, in the Multicenter Automatic Defibrillation Implantation Trial (MADIT), electrophysiology confirmed that inducibility of ventricular tachycardia shows high specificity and a high predictive value for arrhythmic events. Nevertheless, the MADIT study population is not comparable to a cohort of consecutive patients who have recently had a myocardial infarction. In this setting, the highest risk of arrhythmic events can be observed in patients with depressed percent ejection fraction (< 35%) and in the first 6 months after AMI. Today, the most convincing approach seems to be the one combining both noninvasive risk stratification parameters (e.g., premature ventricular beats > 10/h or reduced heart rate variability < 70 ms or a positive signal-averaged electrocardiogram) followed by a further arrhythmic risk stratification, obtained through electrophysiologic study. Several published and ongoing trials that utilize various arrhythmic risk stratification techniques as part of their protocol are reviewed.

Prospective clinical evaluation and follow-up of a cohort of consecutive VT/VF patients, using a staged-care protocol, including coronary arteriography, programmed electrical stimulation and cardiac surgery.

The prospective evaluation and follow-up of 39 consecutive subjects with VT/VF, 6 of whom, with cardiac arrest (CA), are reported. Patients were enrolled in a specific staged-care approach protocol, which included coronary arteriography (CAR) and ventriculography (VC), in order to exclude the need of cardiac surgery, including coronary artery bypass graft (CABG), with and without left ventricular aneurysmectomy (LVA). The protocol included inducibility of VT/VF, which was verified by programmed electrical stimulation (PES) in control conditions and after antiarrhythmic therapy (ADT), to assess persistent inducibility and mainly to verify the hemodynamic sequelae of VT. VT that showed poor hemodynamic tolerance was treated with ICD, while well-tolerated VT was treated by ADT or ablation when indicated. Furthermore, PES was obtained after surgical procedures. As a first step, the patients were assigned to receive amiodarone (AMIO) (200-400 mg/daily) in the presence of EF% < 30% or contraindication to sotalol, (Group A), or sotalol (SOT) (80-140 mg/daily) in the presence of EF > or = 31%. (Group C). Conversely, in case of recurrences, patients were assigned to receive AMIO (200-300 mg/daily) plus metoprolol (MET) (20-100 mg/daily), (Group B) or, in case of intolerance to beta-blockers, to AMIO plus mexiletine (MEX) (200 mg/daily) (Group D). The four groups were similar for the type of VA, with recurrent ventricular tachycardia (RVT) being the most frequent one. The most frequent underlying cardiac disease of VA in this study was post-AMI CAD, with a rate of over 60% in all four groups. Single- and two-vessel lesions were found at CAR in various patients in all four groups, in 5/13 (38%) in Group A, in 8/14 (57%) in Group B, in 5/7 (71%) in Group C, and in 3/5 (60%) in Group D. Cardiac surgery was performed in a similar and limited number of patients in all four groups, in 4/13 (30%) in Group A, in 4/14 (35%) in Group B, in 2/7 (28%) in Group C, and in 2/5 (40%) in Group D. In 8/39 (20.5%) of the patients who underwent CABG, there was no operative or late mortality; 4/39 (10.2%) received CABG and LVA, and two died. For the amiodarone plus metoprolol and sotalol patients only, PES showed a lower residual inducibility, in comparison to the amiodarone and amiodarone + mexiletine groups. In the entire group, 7 out of 26 (27%) were still inducibile at PES while in 19/26 (64%) of the patients, an apparently effective treatment could be found, documenting the relative usefulness of PES. Recurrence rate was the highest in the amiodarone + mexiletine group and in patients with previous CA. Our data show the potential utility and limitations of ADT, even using the most effective antiarrhythmic drugs and association of drugs, mainly because of the high recurrence rate of VT observed in the present study, even in non-inducible patients [14/39 (36%)]. In conclusion, in a prospective and staged-care approach protocol of management of VT/VF patients, only a few patients with VT/VF benefited from cardiac surgery. PES could still play a role in the evaluation of the most effective ADT. Amiodarone + metoprolol seems to be the most effective ADT in these patients. Nevertheless, a high recurrence rate was observed in this patient population, even with an aggressive protocol, in the short follow-up period of 12 +/- 8 months, confirming recent data on the superiority of ICD to ADT, in patients with frequent recurrences or hemodynamically poorly-tolerated VT. In these patients, ICD therapy should definitively be preferred to ADT.

[Clinical characteristics, familial distribution and preliminary genetic data in 9 different families with "Brugada's syndrome"]. / Caratteristiche cliniche, distribuzione familiare e preliminari dati genetici in nove diverse famiglie con "sindrome di Brugada".

Clinical electrocardiographic evaluation and complete non-invasive assessment including nuclear magnetic resonance (NMR) are reported for 7 subjects with cardiac arrest (CA), 6 due to ventricular fibrillation (VF) and 1 to ventricular tachycardia (VT). Two more subjects, one with and one without a family history of non-resuscitated sudden death (NRSD), were included. All 9 subjects showed the typical pattern of the Brugada's syndrome (BS), characterized by incomplete right bundle branch block, ST T elevation in V1 V3. We globally evaluated 64 subjects belonging to the 9 families examined, 5 of whom were identified in Bologna, 3 in Florence and one in Parma. BS is characterized in the experience described in the present paper by a family distribution of the ECG pattern in different members. Furthermore, a family distribution of NRSD, even at a young age, was observed. Electrocardiographic features were consistent with variable degrees and aspects of the intraventricular conduction delay (ICD) and of the ST T elevation pattern. NMR has been performed so far in 23 out of 64 members examined by echo, and was normal in 17/23, with only 6 showing pathological aspects such as mild dilatation of the right ventricle, reduced thickness of the right free wall, isolated dilatation of the right ventricular infundibulum and other minor pathological aspects. Preliminary genetic screening (GS), performed on 20 members of three families, was negative for the typical genetic patterns of right ventricular dysplasia (ARVD). In six families, GS is still ongoing. Genetic screening of sodium channel pathology is in progress in the same families. In conclusion, BS has been documented in the present paper as a hereditary syndrome, both for clinical and ECG aspects, associated with CA due to VF, which required an AICD implantation, at least in symptomatic subjects. There may exist a CONGENITAL form of BS due to pathology of sodium channels, without a demonstrable structural heart disease and an ACQUIRED form of BS secondary to an initial ARVD. From the clinical point of view, a complete evaluation, including serial ECG, pharmacological testing and programmed electrical stimulation of other subjects in the families, may be important in preventing sudden death, mainly in symptomatic subjects who always require an implantable cardioverter defibrillator.