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Background: The impact of diabetes in patients with acute myocardial infarction (AMI) treated with primary percutaneous coronary intervention (PCI) is unclear. The benefit of abciximab in this subset of patients remains controversial., Methods and Results: Three hundred and twenty-seven consecutive and unselected patients with acute AMI treated with primary PCI were included in our single-center retrospective registry, 103 diabetic (31%) and 224 nondiabetic (69%). Abciximab was given at the physician's discretion. Diabetic patients were older (mean age 68.5±11 vs. 65±12 years; P=0.009), had an increased prevalence of hypertension (73 vs. 54%; P=0.001), a decreased prevalence of smoking (31 vs. 45%; P=0.02), a longer duration of symptoms before hospital admission (190 vs. 143 min; P=0.031), and a higher number of stents implanted (1.4 vs. 1.2; P=0.04). Other clinical and angiographic characteristics were comparable in the two groups. Diabetic patients had a higher incidence of the combined end-point of death and reinfarction rate at 30 days (18 vs. 10%; P=0.04) compared to nondiabetic patients. Abciximab treatment was associated with a lower in-hospital (23.8 vs. 5%; P=0.005) and 30-day (23.8 vs. 6.6%; P=0.012) mortality, and a lower incidence of death and reinfarction at 30 days (33.3 vs. 9.8%; P=0.003) in diabetic patients. In nondiabetic patients, abciximab was not associated with improved outcome measures. Advanced Killip class (III and IV) and abciximab were found to be independently associated with 30-day death or myocardial infarction [respectively, odds ratio (OR) 6.075, 95% confidence interval (CI) 1.59-23.218, P=0.008 and OR 0.177, 95% CI 0.034-0.938, P=0.042] in the propensity score-matched populations of diabetic patients. Advanced Killip class and thrombolysis in myocardial infarction score index were found to be independently associated with 30-day death or myocardial infarction (respectively, OR 6.607, 95% CI 1.5-29.106, P=0.013 and OR 1.094 95% CI 1.042-1.148, P<0.001) in the propensity score-matched populations of nondiabetic patients., Conclusions: In our registry diabetic patients treated with primary PCI for AMI had a worse in-hospital and 30-day outcome than nondiabetic patients. Adjunct pharmacologic treatment with abciximab was associated to a better prognosis only in diabetic patients.

Background: With the exception of a few cases such as aborted sudden cardiac death, sustained ventricular tachycardia, and syncope of unexplained origin, there is no consensus on the clinical findings identifying patients with idiopathic dilated cardiomyopathy with an increased risk of sudden cardiac death or malignant ventricular arrhythmias., Methods: To verify whether electrocardiographic and arrhythmologic features could be useful for prognostic stratification, 78 consecutive patients with an invasive diagnosis of idiopathic dilated cardiomyopathy, but without symptomatic ventricular arrhythmias, were enrolled in a prospective study. Signal-averaged ECG, 24 to 48 hour ECG monitoring and electrophysiologic study were performed at the time of diagnosis to identify arrhythmogenic predictors of outcome. Transplant-free and arrhythmic event-free survival was evaluated on the basis of initial parameters., Results: During a mean follow-up of 85 months, 9 patients died (6 of sudden cardiac death and 3 of congestive heart failure), 10 patients underwent cardiac transplantation for refractory heart failure, and 3 presented with sustained ventricular tachycardia. The independent predictors for death and cardiac transplantation were an HV interval > 55 ms and the combination of frequent repetitive ventricular ectopics with a poor left ventricular function. A strong index of arrhythmic events proved to be the association of a prolonged HV interval with a wide (> 110 ms) QRS complex (odds ratio 4.53, 95% confidence interval 1.57-13.04, p < 0.005)., Conclusions: An accurate measurement of the HV interval and QRS duration at baseline evaluation may add prognostic information in patients with idiopathic dilated cardiomyopathy. In our experience, abnormal values of both parameters identified a group of patients with a very high risk of late occurring arrhythmic events.

Background: Transient atrial and appendage dysfunction occurs after cardioversion of atrial fibrillation. It has been suggested that one component of early dysfunction is related to the method of restoration of sinus rhythm and it is less severe in patients undergoing pharmacological than electrical cardioversion. The aim of this study was to compare left atrial chamber and left atrial appendage mechanical function before and after 48 hours from electrical or pharmacological cardioversion in patients with chronic atrial fibrillation., Methods: We studied the effects of the mode of cardioversion on Doppler left atrial and appendage function in 19 patients with persistent atrial fibrillation (> or = 4 weeks), who were randomized to pharmacological (quinidine) or electrical cardioversion (protocol: 200, 300, 360 J) after pre-treatment with verapamil. Transthoracic and transesophageal echocardiography were performed before and 48 hours after the restoration of sinus rhythm. To determine left atrial and appendage mechanical dysfunction, the peak A wave velocities were obtained from transmitral flow velocity profiles recorded in the apical 4-chamber view, and peak emptying and filling appendage velocities were measured by the transesophageal approach with the sample volume placed at the orifice of the left atrial appendage. All the patients were pre-treated with verapamil before cardioversion in order to achieve a satisfactory control of heart rate., Results: Mean peak A wave velocities were 0.52 +/- 0.12 m/s in the patients treated electrically and 0.54 +/- 0.08 m/s in those treated pharmacologically (p = NS). Before and after electrical cardioversion, the peak filling velocities of the left atrial appendage were 0.42 +/- 0.17 and 0.43 +/- 0.17 m/s respectively, and the peak emptying velocities 0.30 +/- 0.14 and 0.36 +/- 0.17 m/s respectively; before and after pharmacological treatment, the peak filling velocities were 0.38 +/- 0.1 and 0.43 +/- 0.1 m/s respectively, and the peak emptying velocities were 0.30 +/- 0.13 and 0.43 +/- 0.24 m/s respectively (p = 0.08)., Conclusions: Even a long period of atrial fibrillation does not lead to a marked depression of global left atrial and left atrial appendage function 48 hours after the restoration of sinus rhythm by means of electrical or pharmacological cardioversion. There is no evidence that electrical cardioversion causes greater post-cardioversion atrial and/or appendage dysfunction than pharmacological treatment after 48 hours. Pre-treatment with verapamil may have reduced the dysfunction (probably because of a reduction in mechanical remodeling during atrial fibrillation).

A spontaneous episode of bundle branch reentry ventricular tachycardia was recorded in a 50 year old man few weeks after operation for a severe aortic valve regurgitation. After surgery, the patient developed recurrent syncope and showed a bradycardia-dependent left bundle branch block and a HV interval of 70 ms. A bundle branch reentry ventricular tachycardia with left bundle branch block morphology, easily induced during premature ventricular stimulation, occurred spontaneously after the longest sinus cycle of a sequence conducted to the ventricles with a left bundle branch block morphology of the QRS complexes. During left bundle branch block an incomplete and concealed anterograde conduction along the left bundle branch was supposed to be present and its disappearance was considered the trigger mechanism of the spontaneous ventricular tachycardia. The negative results obtained with the signal-averaged ECG in our case support the concept that intramyocardial delay is not essential for this type of ventricular tachycardia.

Background: Pharmacological conversion of paroxysmal atrial fibrillation is frequently necessary. The aim of this study was to compare intravenous propafenone, a class Ic antiarrhythmic agent, with placebo in paroxysmal atrial fibrillation (AF) of recent onset (< 72 h)., Patients and Methods: We randomly allocated 75 patients, aged 18 to 70 years, with paroxysmal AF to receive intravenous propafenone (2 mg/kg in 15 min followed by 1 mg/kg in 2 h) or the matching placebo. Patients were followed for 3 h. Exclusion criteria were the presence of one of the following: clinical heart failure, recent acute myocardial infarction, hypotension, atrioventricular block, Wolff-Parkinson-White syndrome, or current treatment with antiarrhythmic agents or digitalis., Results: No sign of heart disease was found in 74.7% of the patients. Echocardiographically determined left atrium diameter was similar in the two groups. Conversion to sinus rhythm occurred in 24 of 41 patients allocated to propafenone and in 10 of 34 patients allocated to placebo (odds ratio 3.2, 95% confidence intervals 1.3-7.9; p < 0.01). Mean conversion time was 34 +/- 29 and 71 +/- 55 min, respectively, for propafenone and placebo. Mean heart rate in nonconverters decreased from 146 to 109 beats/min in patients treated with propafenone while it remained virtually unchanged in those treated with placebo. Only minor side effects were noted., Conclusions: Intravenous propafenone is an effective therapeutic option for restoring sinus rhythm in patients with paroxysmal AF of recent onset.

In a prospective study on 340 cases with primary myocardial disease, eight patients (six males, two females, mean age 36 years, range 24-47) with an idiopathic left ventricular aneurysm were observed. All patients had normal coronary arteries, no angina or history of myocardial infarction; all but one had no risk factors for ischaemic heart disease; all had normal right ventricles; one patient had a history of familial dilated cardiomyopathy, two of 'flu-like' syndrome at the time of first symptom and two of alcohol abuse. All patients had ventricular tachycardia (VT), five sustained (of right bundle branch block morphology in three, and of different morphologies in two), three non-sustained. Patients with sustained VT had inducible VT (resembling the clinical one) on electrophysiological study. Electrocardiogram (ECG) showed an infarction pattern in three cases. Aneurysms were of limited size (2.1 +/- 1/11 segments on echocardiography) and were located in the septum, apex or posterior wall. Left ventricular ejection fraction (LVEF) was reduced (< 0.50) in six patients and was not correlated with the aneurysm size. The duration of illness was inversely correlated with LVEF (P < 0.05). Endomyocardial biopsy showed evidence of diffuse pathological changes in all cases (cell hypertrophy, myofibrillar lysis, mitochondriosis). During follow-up (64 +/- 32 months), patients were successfully treated with anti-arrhythmic drugs: no patients required surgical treatment to control ventricular arrhythmia. Considering the clinical and pathological features of idiopathic left ventricular aneurysm, this primary myocardial disease could be classified as a novel peculiar form of cardiomyopathy.

Right ventricular dysplasia, a heart muscle disease of unknown cause, anatomically characterized by variable replacement of myocardial muscle with adipose or fibroadipose tissue, is usually considered a selective disorder of the right ventricle. However, concomitant left ventricular involvement has been noted in a few cases. The aim of this study was to evaluate the prevalence and characteristics of left ventricular involvement in right ventricular dysplasia, as well as possible progression of the disease. Thirty-nine patients with right ventricular dysplasia were studied by M-mode and two-dimensional echocardiography; 28 of them also underwent cardiac catheterization, and in 25 endomyocardial biopsy was performed. On first examination the left ventricle was normal in 25 patients, whereas in the remaining 14 right ventricular abnormalities were associated with left ventricular involvement, characterized by asynergic areas (12 patients) or diffuse mild hypokinesis (two patients). During follow-up (27 patients, 84.1 +/- 66.1 months) 10 patients showed worsening of right ventricular function; in nine the appearance or worsening of left ventricular abnormalities was observed. Five patients died (four in congestive heart failure and one suddenly). Results of postmortem examination (available in two patients) showed atrophy of myocells and a massive fatty and fibrous infiltration of the right ventricular wall, associated with degenerative changes and fibrosis of the left ventricle. In conclusion, right ventricular dysplasia may be associated with left ventricular involvement and the disorder appears to be progressive in some instances.

Right ventricular cardiomyopathy is generally considered a disease with isolated right ventricular involvement, although there are some case reports of concomitant abnormalities of the left ventricle. In order to evaluate the prevalence, characteristics and natural history of left ventricular involvement in this disease, 39 patients with right ventricular cardiomyopathy were studied by 2-dimensional echocardiography. At first evaluation 25 patients (group 1) showed right ventricular abnormalities and a normal left ventricle. In the remaining 14 patients (group 2) the right ventricular abnormalities were associated with left ventricular involvement (asynergic areas and/or mild diffuse hypokinesia). During the follow-up, left ventricular involvement appeared in 6 patients of group 1 and worsened in 4 patients of group 2. Five patients died. Pathological examination (available in 4 cases) showed, at the level of the right ventricle, marked atrophy of myocytes and fibro-fatty replacement, and predominant fibrosis at left ventricular level. Left ventricular involvement is thus frequent in right ventricular cardiomyopathy. At least in some cases the disease appears to be progressive.

While coronary reperfusion arrhythmias are well defined in animal models, their prevalence and predisposing factors are still uncertain during pharmacologic coronary reperfusion in patients with acute myocardial infarction. In 80 patients, who underwent this procedure and had a continuous electrocardiographic monitoring (associated with a Holter recording in 34), 6 patients developed ventricular fibrillation. Ventricular fibrillation was the terminal event in 2/19 non-reperfused patients. The other episodes of ventricular fibrillation (controlled with DC countershock) occurred within 5 minutes and 3 minutes after angiographic documentation of coronary reperfusion. Ventricular fibrillation was observed in 4/10 patients with a residual stenosis less than or equal to 80% but in no case among the 39 patients with a residual stenosis greater than 80% (P = 0.01). Holter recordings in 19 reperfused patients showed ventricular tachycardia or accelerated idioventricular rhythm at reperfusion in 8/10 patients with a coronary stenosis less than or equal to 80% and only in 3/9 with a higher degree stenosis (P less than 0.05). Reperfusion ventricular fibrillation was found to occur in 8.1% of patients. A residual stenosis of 80% or less was found to be a predisposing factor in the occurrence of ventricular fibrillation, ventricular tachycardia or accelerated idioventricular rhythm at reperfusion.

Ibopamine (SB-7505), the orally active 3,4-diisobutyryl ester of N-methyldopamine, was investigated at doses ranging from 1.09 to 2.34 mg/kg in 12 patients suffering from refractory congestive heart failure. In 7 patients ibopamine produced favorable effects, increasing cardiac index (+35%), stroke volume index (+27%), stroke work index (+30%) and decreasing systemic vascular resistances (-15%), total pulmonary resistances (-20%), pulmonary arteriolar resistances (-28%), whereas in 5 patients it was ineffective. Transient adverse reactions occurred in 3 patients.

In order to clarify the anatomic substrate of idiopathic ventricular tachycardia of right bundle-branch block morphology, responsive to verapamil, two patients with this type of arrhythmia were evaluated using hemodynamic studies, right ventricular endomyocardial biopsy as well as electrophysiological and pharmacological studies. Pressures, right and left ventriculography and coronary angiography were normal in both patients. Case 1 showed a prolonged sinus node recovery time and a histological pattern which was compatible with healed myocarditis. Case 2 presented a complete right bundle-branch block, intra-His conduction defects and histological features of aspecific cardiomyopathy. Our results underline the presence of diffuse ventricular histologic changes in patients with idiopathic ventricular tachycardia of right bundle-branch block morphology. These histologic changes seem unable to interfere with cardiac pump function but are sufficient to create significant abnormalities of impulse formation and conduction.

Risks and complications of arterial hypertension can be reduced by an active and prolonged treatment. However, only a small number of hypertensive subjects is treated effectively. The co-operation of patients in the management of the disease may be useful in the treatment of hypertension. The authors report the results of a study of thirty hypertensive patients chosen at random, who checked their arterial pressure by themselves. The psychological reactions, the advantages and disadvantages of this experience and the attitude of the attending physicians were analyzed. The majority of the patients had no difficulty in the self-measurement of blood pressure and succeeded in reaching and maintaining the values of blood pressure within satisfactory levels, getting favourable psychological effects as well. Six patients (out of the ten who were indifferent or contrary to this practice) went on measuring the arteria pressure, giving in this way a contribution to a better management of the disease. The attitude of the attending physicians was on the whole indifferent or negative towards this experience.

The prognostic value of induction of ventricular tachycardia (VT) by programmed electrical stimulation (PES) was analyzed in 123 patients: 64 (Group I) with spontaneous recurrent VT and 59 (Group II) without a history of serious arrhythmias. Thirty-three patients with spontaneous VT underwent coronary and left ventricular angiography to compare electrical instability with the presence of ventricular disfunction and/or the extent of coronary artery disease (CAD). PES reproducibly induced VT in 49/64 patients with spontaneous VT (sensitivity = 77%) and in 6/59 patients without VT (specificity = 90%). Twenty-two patients (66%) had ventricular disfunction defined by an ejection fraction of less than or equal to 40% or regional wall motion abnormalities. Only 4 patients (33%) had proximal 3-vessel CAD. The mean follow-up period was 16 +/- 12 months. Eight of Group I patients died suddenly and 24 had recurrent symptomatic VT. Three of Group I patients died (1 cardiac failure, 2 non-cardiac deaths), all the survivors were free of serious arrhythmias. In Group I patients mortality was correlated with: recent anterior myocardial infarction, inducible sustained VT with PES, ejection fraction less than or equal to 0.40, ventricular ipoasynergy and or at least one coronary stenosis greater than or equal to 70%. This study suggests that inducible VT is a marker of the risk of sudden death. Electrical instability may occur independent from the etiology of cardiopathy, ventricular disfunction and extent of CAD, but these parameters are correlated to global and sudden mortality in the group of patients with spontaneous VT.

Acute and chronic effects of captopril (C) were studied in 14 patients (12 males, 2 females; mean age 56 +/- 15 years) with chronic congestive heart failure (CCHF) refractory to digitalis and diuretics. All patients underwent hemodynamic evaluation before and after increasing doses of C (6.25-100 mg). Nine patients were evaluated during long term therapy by means of clinical examination, exercise testing, chest-X-ray and echocardiography. After C the following acute haemodynamic changes were observed. Mean right atrial pressure: -25% (p less than 0.01), left ventricular filling pressure: -22% (p less than 0.01), mean systemic arterial pressure: -15% (p less than 0.01), systemic vascular resistance: -31% (p less than 0.01), cardiac index: +36% (p less than 0.01). Of the 9 patients who were evaluated during long term C treatment, 7 (group A, mean follow up 6.4 +/- 4.2 months) improved in 1 or 2 NYHA functional classes and showed an increased exercise tolerance during the first 3-6 months of therapy. In this period, however, two sudden deaths and one drop-out were observed. Moreover, after the seventh month two patients of this group deteriorated clinically. Two patients (group B) developed a progressively weight gain during the first 15 days of C treatment. In the majority of our patients with refractory CCHF, captopril improves cardiac performance in the acute phase and in the first 3-6 months of therapy. Controlled studies and longer follow up are needed to understand better the long term effects of C in CCHF patients.