BackgroundThe independent prognostic impact of diabetes mellitus (DM) and prediabetes mellitus (pre‐DM) on survival outcomes in patients with chronic heart failure has been investigated in observational registries and randomized, clinical trials, but the results have been often inconclusive or conflicting. We examined the independent prognostic impact of DM and pre‐DM on survival outcomes in the GISSI‐HF (Gruppo Italiano per lo Studio della Sopravvivenza nella Insufficienza Cardiaca‐Heart Failure) trial.Methods and ResultsWe assessed the risk of all‐cause death and the composite of all‐cause death or cardiovascular hospitalization over a median follow‐up period of 3.9 years among the 6935 chronic heart failure participants of the GISSI‐HF trial, who were stratified by presence of DM (n=2852), pre‐DM (n=2013), and non‐DM (n=2070) at baseline. Compared with non‐DM patients, those with DM had remarkably higher incidence rates of all‐cause death (34.5% versus 24.6%) and the composite end point (63.6% versus 54.7%). Conversely, both event rates were similar between non‐DM patients and those with pre‐DM. Cox regression analysis showed that DM, but not pre‐DM, was associated with an increased risk of all‐cause death (adjusted hazard ratio, 1.43; 95% CI, 1.28–1.60) and of the composite end point (adjusted hazard ratio, 1.23; 95% CI, 1.13–1.32), independently of established risk factors. In the DM subgroup, higher hemoglobin A1c was also independently associated with increased risk of both study outcomes (all‐cause death: adjusted hazard ratio, 1.21; 95% CI, 1.02–1.43; and composite end point: adjusted hazard ratio, 1.14; 95% CI, 1.01–1.29, respectively).ConclusionsPresence of DM was independently associated with poor long‐term survival outcomes in patients with chronic heart failure.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00336336.

Although human baroreflexes are known to exert a powerful physiological control on heart rate, little information exists on the physiological control they exert on the atrioventricular conduction system. In 11 normotensive subjects with normal atrioventricular conduction, we altered baroreceptor activity by injection of pressor and depressor drugs (phenylephrine and trinitroglycerin) and recorded mean arterial pressure (MAP, catheter measurements), R-R interval, and pre-His and post-His intervals (A-H and H-V, His bundle recording). With the subjects in sinus rhythm, increasing MAP by 21+/- 1 mm Hg caused a marked lengthening (250 +/- 28 msec), and decreasing MAP by 17 +/- 2 mm Hg a marked shortening (142 +/- 16 msec) of the R-R interval. There was little change in the A-H interval and no change at all in the H-V interval. However, when the R-R interval was kept constant in these subjects by atrial pacing, a similar increase and decrease in MAP caused, respectively, a marked lengthening (49 +/- 6 msec) and shortening (19 +/- 3 msec) of the A-H interval, although the H-V interval remained unaffected. Thus physiological ranges of baroreceptor activation have a marked influence on the atrioventricular node but apparently not on the ventricular portion of the atrioventricular conduction system. This influence is unmasked when pacing prevents the baroreceptor influence on the sinoatrial node.

The demonstration of extensive coronary artery disease (CAD) after acute myocardial infarction (AMI) has important prognostic implications. Exercise-induced ST segment depression is commonly used for detecting the presence of CAD and evaluating its extension. However, even though there have been many attempts to increase its diagnostic yield, the accuracy of the electrocardiographic signal for identifying multivessel disease (MVD) is relatively low, particularly in post-MI patients. The aim of this study was to evaluate the ability of a simple index, combining information on the amount and kinetics of ST depression in the heart rate domain during exercise and recovery, to identify MVD after AMI. Seventy patients (mean age 53.4 years) underwent a bicycle, symptom-limited exercise stress test and coronary angiography 2-3 weeks and 6 weeks respectively, after uncomplicated AMI while cardioactive therapy was discontinued. After obtaining a computer-derived measurement of ST levels based on incremental averaging of normal complexes, the area subtended to baseline and limited by the ST trend against heart rate during both exercise (A1) and recovery (A2) was calculated. The difference (A1-A2) was defined as the 'Stress-Recovery Index' (SRI) and dichotomized, by means of receiver-operating characteristics curve analysis, at 5 mm x beats.min-1 to define an increased risk of MVD. The SRI of patients with MVD was significantly lower than that of patients with single vessel disease. The sensitivity of SRI < -5 mm x beats.min-1 (65%) for predicting MVD was significantly higher than that obtained by other conventional parameters, without appreciable loss of specificity (81%).(ABSTRACT TRUNCATED AT 250 WORDS)

Streptokinase treatment of AMI causes abrupt activation of the complement system, whereas no significant complement activation can be detected in plasma of AMI patients not treated with fibrinolytic agents. Complement activation causes a transient leukopenia, as reported for such other clinical conditions as dialysis and cardiopulmonary bypass, and possibly contributes to the hypotension observed during streptokinase treatment.

We performed a prospective study of the high‐frequency components of the terminal portion of the QRS complex in 220 patients who survived acute myocardial infarction. Signal‐averaged electrocardiograms (SA‐ECGs) were performed before hospital discharge (16 ± 6 days) and then serially at regular intervals over the following year. SA‐ECGs were processed using a 40 Hz high‐pass bidirectional filter. Duration of “filtered” QRS (D‐normal value < 120 ms), duration of the low‐amplitude signals. (D40 ‐ n.v. < 39 ms) and last 40 ms voltage of the QRS complex (V40 ‐ n.v.> 20 µV) were measured. Late potentials (LPs) were defined as the presence of two or more abnormal values. In addition, 24‐hour Holter monitoring was performed in 208 patients and left ventricular ejection fraction (LVEF) was determined by scintigraphy in 111. Sixty‐two patients (group 1) had LPs, 158 had normal SA‐ECGs (group 2). Spontaneous normalization of SA‐ECGs occurred in 20% of patients after 6 months, although the mean values of D, D40 and V40 did not change significantly and the reproducibility was very good for all the indexes during all the follow‐up controls. Three patients had sudden death and three presented again with spontaneous, sustained ventricular tachycardia. Five of 62 (8%) group 1 patients had an arrhythmic event compared with one of 158 patients (0.6%) in group 2. The sensitivity of SA‐ECGs as a predictor of arrhythmic events was 83% with a specificity of 73%. Patients with subsequent arrhythmic events had longer filtered QRS (133 ± 19 vs 104 ± 16 ms; P < 0.001), longer duration of the low‐amplitude signals (54 ± 15 vs 33 ± 14 ms; P < 0.01), and lower voltages in the last 40 ms of the filtered QRS (11 ± 3 vs 36 ± 25 µV; P < 0.02) and, moreover, higher peak CK values and lower LVEF than those without such events. In conclusion, SA‐ECGs provide important prognostic information in identifying patients at risk of arrhythmic events after myocardial infarction although dynamic changes of LPs are observed during the first year after myocardial infarction.