Predictive models of surgical site infections after coronary surgery: insights from a validation study on 7090 consecutive patients.

BACKGROUND: The role of specific scoring systems in predicting risk of surgical site infections (SSIs) after coronary artery bypass grafting (CABG) has not been established. AIM: To validate the most relevant predictive systems for SSIs after CABG. METHODS: Five predictive systems (eight models) for SSIs after CABG were evaluated retrospectively in 7090 consecutive patients undergoing isolated (73.9%) or combined (26.1%) CABG. For each model, accuracy of prediction, calibration, and predictive power were assessed with area under receiver-operating characteristic curve (aROC), the Hosmer-Lemeshow test, and the Goodman-Kruskal γ-coefficient, respectively. Six predictive scoring systems for 30-day in-hospital mortality after cardiac operations were evaluated as to prediction of SSIs. The models were compared one-to-one using the Hanley-McNeil method. FINDINGS: There were 724 (10.2%) SSIs. Whereas all models showed satisfactory calibration (P = 0.176-0.656), accuracy of prediction was low (aROC: 0.609-0.650). Predictive power was moderate (γ: 0.315-0.386) for every model but one (γ: 0.272). When compared one-to-one, the Northern New England Cardiovascular Disease Study Group mediastinitis score had a higher discriminatory power both in overall series (aROC: 0.634) and combined CABG patients (aROC: 0.648); in isolated CABG patients, both models of the Fowler score showed a higher discriminatory power (aROC: 0.651 and 0.660). Accuracy of prediction for SSIs was low (aROC: 0.564-0.636) even for six scoring systems devised to predict mortality after cardiac surgery. CONCLUSION: In this validation study, current predictive models for SSIs after CABG showed low accuracy of prediction despite satisfactory calibration and moderate predictive power.

Surgical resection of right coronary artery stenoses.

A right coronary artery stenosis was resected in eight patients during multivessel operations. The artery was reconstructed by end-to-end anastomosis, restoring a normal antegrade pathway. All patients recovered uneventfully and remain asymptomatic at follow-up.

Electrocardiography of myocarditis revisited: clinical and prognostic significance of electrocardiographic changes.

To clarify the clinical and prognostic value of the ECG, an ECG review was undertaken in 45 consecutive patients with a histologic diagnosis of active myocarditis (29 men and boys and 16 women and girls; age, 36.8 +/- 15 years; idiopathic myocarditis, 39 cases). In patients (21) with symptoms of recent onset (less than or equal to 1 month) AV block and repolarization abnormalities were the prevailing ECG features at the time of admission, and a pseudoinfarction pattern (Q waves plus ST-segment elevation) frequently heralded a rapidly fatal course ("fulminant myocarditis"). Left atrial enlargement and atrial fibrillation, left ventricular hypertrophy and LBBB, which prevailed in patients who had symptoms for longer periods, corresponded to the most severe degree of left ventricular dysfunction during the initial hemodynamic and echocardiographic evaluation. The overall mortality rate after 58 +/- 24 months from the time of diagnosis was 29%. Abnormal QRS complexes and LBBB were markers of poor survival, independently of initial indexes of left and right ventricular function, both of which indicate an increased propensity for sudden cardiac death.

The use of associated propafenone in patients with amiodarone-resistant ventricular tachycardia.

To clarify the risk-benefit ratio involved in association of antiarrhythmic drugs, a combined therapy of amiodarone and propafenone was tested by means of continuous electrocardiographic monitoring, analysis of levels of the drug in the plasma and programmed electrical stimulation in a selected group of 10 patients who had left ventricular dysfunction and spontaneous relapses of sustained ventricular tachycardia despite treatment with amiodarone. Induction of sustained ventricular tachycardia, possible in each case during treatment with amiodarone, was suppressed after addition of propafenone in 2 patients (responders), who had the best ejection fractions of the entire group (greater than 45%). Worsening of spontaneous tachycardias developed in 4 cases during the combined therapy. These ventricular arrhythmias, although generally at a low rate, sometimes had the potential to degenerate into ventricular fibrillation and disappeared after both discontinuation of propafenone or increase of its dosage (1 patient). Of the six cases undergoing chronic combined treatment, only the responders to premature electrical stimulation were completely protected from recurrences of arrhythmia. Three cases, on the other hand, needed permanent endocardial pacing for symptomatic bradyarrhythmias. The combination of treatment with amiodarone and propafenone, although potentially useful in limiting dosages of and toxicity from amiodarone, is frequently associated with undesirable, and occasionally has severe, side-effects. The best candidates for this pharmacological association seem to be patients without severely depressed left ventricular function who have a greater probability of not presenting the inducibility of ventricular tachycardia after the addition of propafenone to the regimen for treatment.

Immunosuppressive treatment in myocarditis.

Twenty patients (13 males and seven females) with a biopsy-proven diagnosis of myocarditis underwent a period of treatment with prednisone and azathioprine. The primary objective of the study was the observation of histologic changes which occur during treatment and after treatment withdrawal. The secondary objective was the detection, if any, of changes in left ventricular ejection fraction. Multiple endomyocardial biopsies were obtained and the treatment was adjusted in order to achieve complete disappearance of the myocardial inflammation. The histologic status was improved in all patients, although complete disappearance of the signs of active disease was seen in 15 patients only. Two patients died during the observation period. A clear relationship between histologic status and immunosuppression was established in some patients (50% of all cases showed a worsening after withdrawal from the treatment). An overall improvement of the ejection fraction was observed (from 0.37 +/- 0.14 to 0.46 +/- 0.17), but a direct effect of the treatment on the recovery of ventricular function cannot be stated. In some patients, however, a direct relationship between the histological changes and the changes in ejection fraction was seen. These data suggest that treatment with prednisone and azathioprine may be beneficial in some patients with biopsy-proven myocarditis and depressed ventricular function.

Echocardiographic findings in myocarditis.

This study analyzes morphologic and functional alterations detected by M-mode and 2-dimensional echocardiography in 41 patients with histologically proven myocarditis and different clinical presentations: congestive heart failure (63%), atrioventricular block (17%), chest pain (15%) and supraventricular arrhythmias (5%). Left ventricular dysfunction was common (69%), particularly in patients with congestive heart failure (88%), often without or with minor cavity dilatation. Patients with atrioventricular block or chest pain had usually preserved ventricular function. Right ventricular dysfunction was present in 23%. Additional findings included asynergic ventricular areas (64%), left ventricular "hypertrophy" sometimes reversible (20%), hyperrefractile myocardial areas (23%), ventricular thrombi (15%) and "restrictive" ventricular filling (7%). It is concluded that echocardiographic features of myocarditis are polymorphous and nonspecific. The echocardiographic pattern can simulate alternatively dilated, hypertrophic, restrictive or "right" ventricular cardiomyopathy, as well as coronary artery disease. In an appropriate clinical context, echocardiography can be helpful in the diagnosis of myocarditis and in the selection of patients for endomyocardial biopsy.

[Cardiac amyloidosis. Invasive and noninvasive diagnosis]. / Amiloidosi cardiaca. Diagnosi invasiva e non invasiva.

Aim of this study is the analysis of clinical, morphologic and haemodynamic features of cardiac amyloidosis. Cardiac amyloidosis was demonstrated histologically in 7 of our patients: in 6 by endomyocardial biopsy during cardiac catheterization, in one at autopsy. The clinical picture was characterized in every patient by signs and symptoms of congestive heart failure. The electrocardiogram showed several non specific signs: low voltage of the QRS complexes, both in peripheral (4/7) and precordial leads (7/7 cases); marked leftward and upward deviation of the QRS axis (6/7 cases); first degree A-V block (5/7); abnormal Q waves (7/7). M-mode and two-dimensional echocardiography invariably demonstrated a typical pattern: a non dilated left ventricle with thickened and hyper-refractile walls, and usually a slight-moderate diffuse hypokinesia. Other common features were a thickening of right ventricular walls, interatrial septum, and atrioventricular and semilunar valves. Computerized analysis of the M-mode tracings disclosed a marked impairment of the indexes of both systolic and diastolic ventricular function in all patients. By correlating electrocardiographic and echocardiographic data, we found in every case a striking disproportion between the low QRS voltage and the high muscle cross-sectional area (an echocardiographic index of left ventricular mass): this pattern appears to be highly suggestive of infiltrative heart disease. Cardiac catheterization (performed in 6 cases) showed an increase of left ventricular (6/6) and right ventricular (5/6) end-diastolic pressure, with a dip plateau pattern in some cases (4/6 of the left, 2/6 in the right ventricle). The cardiac index was decreased in 3/6 cases. Left ventricular angiography confirmed the echocardiographic data of normal volumes and a slight-moderate decrease of the ejection fraction. We conclude that cardiac amyloidosis usually mimics a restrictive cardiomyopathy (severe congestive heart failure with increased ventricular filling pressures, in the absence of severe systolic ventricular dysfunction). This disease can be suspected clinically by the correlation of the clinical, electrocardiographic and echocardiographic data. The final diagnosis requires an endomyocardial biopsy.