Causes and prognosis of cardiac arrest in a population admitted to a general hospital; a diagnostic and therapeutic problem.

BACKGROUND: The purpose of this study was to determine the causes and the prognosis of consecutive patients resuscitated from cardiac arrest occurring in a general hospital. We assessed 28 females and 94 males (aged 13-82 years) who were resuscitated from cardiac arrest not attributable to acute myocardial infarction. Ventricular fibrillation (VF) was documented in 97. Non-cardiac causes were excluded. Non-invasive studies (24 h Holter monitoring, 2D echocardiogram, signal-averaged ECG, exercise testing, magnetic resonance imaging) and invasive studies (right and left ventricular angiography, coronary angiography and complete electrophysiologic study (EPS) were performed. RESULTS: An underlying cardiac disease was found in 107 patients (88%). Patients were followed for a period ranging from 6 months to 10 years (mean 4+/-5 years). Several causes for cardiac arrest were identified and treated specifically. The prognosis was variable. Among surviving patients the following causes of cardiac arrest were found: Wolff-Parkinson-White syndrome (n=2), rapid supraventricular tachycardia (n=6), acquired or congenital long QT syndrome (n=7), complete atrioventricular block (n=3), proarrhythmic effect of an antiarrhythmic drug (n=5), vasospastic angina (normal coronary arteries) (n=5). Among ten patients with VF related to cardiac ischaemia two died suddenly. Ventricular tachycardia (VT) or VF was the main cause leading to resuscitation after cardiac arrest (n=64). The risk of recurrence of arrest is confirmed in the present study particularly in patients in whom VT/VF could not be suppressed by antiarrhythmic drug therapy (n=45) and in those where an ICD was not implanted (18 cardiac deaths (nine sudden cardiac deaths (SCD's)). The cause of cardiac arrest was not elucidated in 20 patients (16%). The prognosis of these patients differed according to the documentation of VF at the time of cardiac arrest: of those with documented VF (n=12), six patients died suddenly (one with an ICD); of those without documented VF (n=8), all are alive. CONCLUSION: To determine the precise cause of cardiac arrest was the first problem; the diagnosis of cardiac arrest clearly was erroneous in 8 of 122 patients (6.5%). In other patients, a ventricular tachyarrhythmia was identified as the cause for cardiac arrest in half of the population; the indication for an ICD is evident in this group. In 31% of patients with proven cardiac arrest, another arrhythmia requiring specific treatment was identified and ICD implantation was avoided; these patients had a survival of 92% at 3 years. In patients without an identified cause of cardiac arrest and negative EPS, the prognosis was unfavorable only in those with documented VF.

Postoperative ventricular arrhythmias after cardiac surgery: immediate- and long-term significance.

AF is frequent after cardiac surgery. However, ventricular arrhythmias are less known. The purpose of the study was to evaluate the causes and the prognostic significance of severe ventricular arrhythmias occurring after cardiac surgery. For 10 years, among 2,100 cardiac surgeries, 16 (0.8%) patients (13 men, 3 women; age 49-71 years, mean 62 +/- 9 years) without previous ventricular arrhythmias, with preserved left ventricular ejection fraction, and without acute cause of ventricular arrhythmias, developed VF (n = 4) or a sustained VT between 3 days and 3 weeks after cardiac surgery (coronary artery bypass grafting [n = 6], valve replacement [n = 10]). Rapid AF (n = 5) or slow AF (n = 1) were present at the time of VT/VF. Programmed ventricular stimulation occurred after up to three extrastimuli in the basal state and after infusion of 20-30 micrograms of isoproterenol. An echocardiogram, coronary angiography, Holter monitoring with heart rate variability (HRV) study were performed. Ventricular stimulation was negative in six patients (with AF); sustained and clinical VT was induced in 10 patients with a left ventricular ejection fraction > 0.40, except in one patient. Valvular prothesis and coronary bypass graftings were normal. In all patients, HRV was normal before surgery and decreased after cardiac surgery; before versus after surgery, respectively, HR 69 +/- 9 and 89 +/- 30 beats/min (P < 0.01), SDNN 117 +/- 31 and 50 +/- 11 ms (P < 0.001), low frequency (LF) 474 +/- 658 and 51 +/- 40 ms2 (P < 0.05), high frequency (HF) 115 +/- 23 and 33 +/- 32 ms2 (P < 0.05), LF:HF 4 +/- 3 and 1 +/- 0.6 (P < 0.01). Follow-up lasted from 6 months to 10 years (mean 3 +/- 2 years). In patients without induced VT, 1 patient died from asystole, 1 had an ICD but no subsequent events, and the other 4 untreated patients are free of events. Patients with induced VT were treated with amiodarone and beta-blockers except in one patient who died from extracardiac complications. Six of nine patients had no inducible VT with this treatment and are alive; 3 patients had inducible VT, 1 died suddenly before implantation of ICD, and 2 patients are alive with an ICD; recurrent VTs were noted in one patient and received an ICD. In conclusion, recent heart surgery may increase the risk of ventricular arrhythmias. The reduction of indexes reflecting sympathetic and parasympathetic tone could facilitate the occurrence of atrial arrhythmias (and then VT) in patients without ventricular arrhythmogenic substrate or the development of VT/VF in patients with a latent previous ventricular arrhythmogenic substrate. In patients without inducible VT, the prognosis is excellent and an ICD is not recommended in these patients. In those with inducible VT, there is a high incidence of responders to antiarrhythmic drugs with a favorable prognosis.

Echocardiography improves detection of rejection after heterotopic mouse cardiac transplantation.

BACKGROUND: Current assessments of cardiac rejection in murine transplant models rely on subjective estimates of the force of the palpable heart beat that have limited sensitivity and precision. METHODS: We used 2-dimensional echocardiography to evaluate changes in left ventricular posterior wall thickness (PWT) in a heterotopic cardiac mouse transplant model of rejection. Nine allografts and 6 isografts were imaged daily for 6 days and harvested. Thirteen allografts were imaged daily and harvested at day 3. RESULTS: Intraobserver variability on PWT was 0.003 +/- 0.09 mm, interobserver variability 0.09 +/- 0.11 mm. Allograft PWT increased after transplantation (0.74 +/- 0.02 mm to 1.28 +/- 0.05 mm at day 5, P <.0001). For isografts, PWT remained constant (0.73 +/- 0.03 mm to 0.85 +/- 0.01 mm) after an initial increase at day 1. Palpation failed to identify rejection at day 3 whereas PWT was already increased (1.15 +/- 0.02 mm in the allografts at day 3 vs 0.85 +/- 0.02 mm in the isografts, P <.0001). There was a relation between histologic score and PWT (P <.0001). CONCLUSION: Two-dimensional echocardiography allows the noninvasive detection and follow-up of cardiac rejection after transplantation. It eliminates the subjectivity of palpation and provides quantitative and reliable indices of rejection.

Pulse inversion harmonic imaging improves endocardial border visualization in two-dimensional images: comparison with harmonic imaging.

Pulse inversion harmonic imaging (PIHI) is a new modality that increases the detection of harmonic echoes and myocardial contrast by cancelling linearly transmitted signals. We tested whether PIHI improved the detection of endocardial borders in noncontrast 2-dimensional echocardiography. We compared PIHI with tissue harmonic imaging (THI), which decreases linearly transmitted signals using filters. Fundamental mode (FM) was compared with THI and PIHI in 50 consecutive patients. The global and segmental endocardial visualization scores measured with FM were significantly improved by using either THI or PIHI. The improvement of the global score compared with FM was slightly higher using PIHI than THI, because of an improved visualization of the base and the anterior wall with the PIHI technique compared with THI. The ratio of myocardial-to-cavity signal was similarly increased from FM with THI and PIHI. PIHI, a new modality for detection of myocardial contrast, can also be used for endocardial border visualization. It provides an improvement relative to THI for specific regions of the endocardium.