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Aim of our work was to validate magnetic resonance angiography (MRA) in detecting occlusion/patency of coronary artery bypass grafts. Twenty patients with previous history of bypass surgery and recurrent episodes of chest pain were enrolled. Two patients could not be studied (claustrophobia, erratic breathing). Thus, 18 patients with 51 bypasses were examined using a navigator echo sequence: 21 arterial grafts (six sequential) and 30 saphenous vein grafts (five sequential). All patients had undergone contrast conventional angiography 3-15 days before MRA. The magnetic resonance (MR) data set was analyzed by two independent readers blinded to the results of conventional angiography (occlusion of 12 of 51 grafts). At magnetic resonance, two bypasses of the posterior descending artery, patent at conventional angiography, could not be visualized because of imaging slab malpositioning. Interobserver concordance was 96% (47/49). Magnetic resonance and conventional angiography provided identical answers in 47 out of 49 (96%) of the examined grafts. Eleven out of 12 occluded grafts and 36 out of 37 patent grafts were correctly identified with MR. As far as occlusion is concerned, the sensitivity of MR was 91%, the specificity 97%. To summarize, a 30 min outpatient MR examination is highly reliable in determining occlusion/patency of arterial and venous, single and sequential bypasses.

We reevaluated the magnetic resonance (MR) examinations of 38 healthy volunteers (control group, CG) and of 124 patients with RV arrhythmia with left bundle branch block (LBBB) morphology: 45 with episodes of RV sustained tachycardia and of polymorphic RV premature beats (RVST-PPB group); 36 with only RV outflow tract sustained or not sustained tachycardia (RVOTT group); 43 with RV monomorphic premature beats (RVMPB group). All the examinations were reevaluated in a blinded fashion for detecting myocardial adipose replacement (AR) and wall bulges or aneurysms. In RVST-PPB patients, no AR was observed in 9%; 1 RV region involvement, 0%; 2 regions, 4%; > or = 3 regions, 87%; left ventricle (LV), 15%. RVOTT patients: 28%, 53%, 14%, 5%, and 0% [corrected], respectively. RVMPB patients: 33%, 46%, 19%, 2%, and 0% [corrected], respectively. In CG, AR was observed in 11% (in RV outflow tract), RV bulges were detected in 75% [corrected] of RVST-PPB, 39% of RVOTT, and 14% of RVMPB patients, none of the CG; RV aneurysms in 33% of RVST-PPB patients, none of RVOTT patients, RVMBP patients, and CG. A significant difference among groups for RV and LV AR as well as RV bulges and aneurysms was found (p < 0.0001). In the direct comparisons, significant differences were found for: disease duration (RVST-PPB vs. RVMPB, p = 0.0396); RV AR (all the patients groups vs. CG, RVST-PPB vs. RVOTT or RVMPB, p < 0.0001); RV aneurysms (RVST-PPB vs. CG, RVST-PPB vs. RVOTT or RVMPB, p < 0.0002); bulges (all comparisons, p < 0.0174). AR is confirmed as a structural substrate in RV arrhythmias. Number and extension of MR abnormalities are correlated to different degrees of RV arrhythmias.

To evaluate left ventricular myocardial mass and function as well as ostial coronary artery cross-sectional area in endurance athletes, an athlete group of 12 highly trained rowers and a control group of 12 sedentary healthy subjects underwent MR examination. An ECG-gated breath-hold cine gradient-echo sequence was used to calculate myocardial mass, end-diastolic and end-systolic volumes, stroke volume, and cardiac output, all related to body surface area, as well as ejection fraction. A 3D fat-saturated ECG- and respiratory-triggered navigator echo sequence was used to evaluate coronary arteries: left main (LM), left anterior descending (LAD), left circumflex (LCx), and right coronary artery (RCA). Cross-sectional area was calculated and divided for body surface area. Myocardial mass was found significantly larger in athlete group than in control group (p = 0.0078), the same being for end-diastolic volume (p = 0.0078), stroke volume (p = 0.0055), LM (p = 0.0066) and LAD (p = 0.0129). No significant difference was found for all the remaining parameters. Significant correlation with myocardial mass was found for LM (p < 0.001) and LAD (p = 0.0340), not for LCx and RCA. Magnetic resonance imaging is a useful tool in evaluating the myocardial hypertrophy and function of athlete's heart. Magnetic resonance angiography is a valuable noninvasive method to visualize the correlated cross-sectional area increase of the left coronary artery system.

We have examined the effects of 6 months of treatment with growth hormone (GH) (0.02 U/kg/day) in 10 patients with chronic postischemic cardiac failure. Ten patients matched for age, body mass index, functional class, and ejection fraction served as a control group. In the GH group, 1 patient died and 2 were withdrawn from the study because of arrhythmia or worsening of heart failure. In the control group, 1 patient died and 1 patient was withdrawn from the study because of progressive heart failure. Among GH patients, those with an unfavorable outcome had a greater left ventricular end-diastolic diameter (79, 82, and 88 mm) on entry to the study than patients without adverse events (range 62 to 72 mm). At the end of the study, the seven GH patients reported a feeling of well-being and had a significant increase in their exercise test duration (462 +/- 121 vs 591 +/- 105 seconds, p <0.05). Low baseline insulin-like growth factor-I values were increased with GH treatment (189 +/- 52 vs 100 +/- 22 ng/ml, p <0.01). GH did not change left ventricular diameters or wall thickness. A trend toward decreased serum triglyceride levels and adipose body tissue associated with an increase in high-density lipoproteins was observed in the GH group. In conclusion, our present data support previous suggestions that GH treatment exerts some beneficial effects in patients with chronic, stabilized, moderately severe heart failure, but may have deleterious effects in patients with more severe heart failure.

The increasingly widespread use of myocardial revascularization by aortocoronary bypass grafts and the frequent need for their angiographic control require noninvasive imaging procedures able to provide reliable information on their performance. After an overview of angiography as gold standard and the different imaging procedures of aortocoronary bypass grafts alternative to MRI, echocardiography, nuclear cardiology, X-ray or electron beam ultrafast CT, main MRI procedures for the study of aortocoronary bypass, are illustrated together with the results of the personal experience as those of navigator echo technique provided with cardiac and respiratory synchronization (91% sensitivity for aortocoronary bypass occlusion and 97% specificity for patency). In the near future, hardware and software refinements, intravascular contrast media and the application to aortocoronary bypass grafts of flowmetric techniques of phase-velocity mapping will enable the evaluation of bypass stenosis and distal coronary arteries as well as a complete functional graft assessment.

The aim of our study was to define cardiac morphological and functional abnormalities of right ventricular dysplasia by magnetic resonance imaging. Twenty-two healthy volunteers (age, 37.7 +/- 14.2 years) free of cardiac or respiratory diseases (group I) and 12 patients (age, 41.9 +/- 15.8 years) with clinical, electrophysiological and cineangiographic diagnosis of right ventricular dysplasia (group II) underwent magnetic resonance imaging at 0.2 Tesla. End-diastolic diameter, trabecular disarray and segmental wall motion abnormalities were evaluated for the right ventricle as were adipose replacement and fractional shortening for both ventricles. The right ventricular end-diastolic diameter was significantly enlarged in group II (P = 0.0023). Right ventricular trabecular disarray was mild in two group I subjects, and moderate in seven and massive in five group II patients. Right ventricular systolic bulges were found in seven group II patients, aneurysms in five. Excellent agreement was found between magnetic resonance imaging and cineangiography for bulges, aneurysms and tricuspid regurgitation (P < 0.0001). On spin-echo images, signal hyperintensities, due to adipose replacement, were found in 44 cardiac regions in group II: right ventricular outflow tract (12), sub-tricuspid posterobasal region (8), right ventricular apex (9), right ventricular anterior wall (6), interventricular septum (4), left ventricular lateral wall (4), left ventricular apex (1). Significant signal-to-noise ratio differences were found between group II abnormal areas and group I myocardial tissue for the right (P < 0.0001) and left ventricles (P = 0.0006). Fractional shortening in the right and left ventricles were significantly reduced in group II (P = 0.0002 and P = 0.00016, respectively). Magnetic resonance imaging can be considered a very useful diagnostic tool for the detection of features typical of right ventricular dysplesia, such as adipose replacement, trabecular disarray, bulges and aneurysms and provides useful information about cardiac function and regional wall motion. It indicates that left ventricular involvement occurs in a significant fraction of patients, and suggests that right ventricular dysplasia may be a generalized cardiomyopathy.

The effect of L-propionylcarnitine on patients with left ventricular dysfunction (EF < 45%) NYHA class II, symptomatic despite therapy with digitalis and diuretics was evaluated in a phase II parallel, double-blind, randomized, placebo-controlled study. Fifty patients (28 men and 22 women) aged 37-70 years received 1.5 g of L-propionylcarnitine or placebo on a random basis as oral treatment for 6 months. At baseline, during a 7 day placebo run-in period, and during the 6-month treatment bicycle exercise test, M-B mode and Doppler echocardiography, and clinical evaluation (clinical score) were repeatedly performed. The analysis of variance for repeated measurements showed a statistically significant difference (P < 0.01) in the mean value of exercise time between the treatments over the period of the study. There was a final increase of 0.36 min in the placebo group, 1.4 min in the treated group and a minor production of lactate during exercise in the treated group. Left ventricular shortening fraction and left ventricular ejection fraction showed a significant increase in the L-propionylcarnitine group (respectively P < 0.01 and P < 0.0001) whereas no difference was apparent in the placebo group. Stroke volume index and cardiac index showed significant increments in the treated group (P < 0.05) and systemic vascular resistance was lowered (P < 0.05). No haemodynamic variations were observed in the placebo group, and the clinical score showed a significant improvement in the L-propionylcarnitine treated group. In conclusion, L-propionylcarnitine treatment was shown to improve patient symptomatology and effort tolerance.

Objective: We compared MRI with two-dimensional echocardiography (2dE) and Doppler echocardiography to determine the diagnostic role of MRI in hypertrophic cardiomyopathy (HCM)., Materials and Methods: Twenty-three patients with 2dE diagnosis of HCM were examined with MRI; 12 of 23 patients were also studied by color (cDE) and continuous wave (cwDE) Doppler echocardiography. Morphologic information and diastolic heart wall thickness were obtained by SE sequences; functional study was performed by gradient echo sequences (cine MR)., Results: The correlation between MR, SE sequences and 2dE was better for septal (r = 0.930, p < 0.01) than for posterolateral (r = 0.739, p < 0.01) wall thickness. The assessment of the distribution of the hypertrophy was changed by MR in five cases. Cine MR functional study showed a systolic subaortic signal void (dynamic obstruction) in 12 of 22 patients and a systolic left atrial signal void (mitral regurgitation) in 17 of 22. Systolic wall thickening was studied by cine MR and 2dE in 11 patients: A good correlation was found for septum (0.01 < p < 0.05) and a poor one for posterolateral wall (p > 0.05). The cine MR and cDE turbulence duration in the left ventricle and atrium showed excellent correlation (p < 0.01). Good agreement was found between the duration of subaortic turbulence (cine MR or cDE) and the pressure gradient (cwDE) (p < 0.01 and 0.01 < p < 0.05, respectively) and between cine MR and cDE semiquantitative estimate of the mitral regurgitation (p < 0.01). In all patients with subaortic MR signal void studied with cwDE, a pressure gradient was present., Conclusion: Magnetic resonance imaging can play an important role in the diagnosis of HCM after 2dE-DE.

Patients with symptomatic myocardial ischaemia received amlodipine (once daily) or diltiazem (three times daily) for 10 weeks. Amlodipine and diltiazem showed comparable efficacy in reducing angina attack rates and glyceryl trinitrate consumption. Amlodipine produced a significantly greater reduction in the mean rate pressure product. Both drugs were well tolerated with only mild side effects occurring at the higher doses. In two cases, side effects were also reported at the lower dose of diltiazem (30 mg three times daily); none occurred with the 5-mg daily dose of amlodipine. In the overall clinical assessment, efficacy of amlodipine was considered excellent in 100% of cases as compared with 40% for diltiazem. Amlodipine is clearly effective when administered once daily for the treatment of myocardial ischaemia.

The efficacy and safety of amlodipine (5-10 mg once daily) and diltiazem (30-60 mg three times daily) were compared in 40 patients with symptomatic myocardial ischemia. A 2-week placebo run-in period was followed by 10 weeks of open treatment with amlodipine (n = 20) or diltiazem (n = 20). Concomitant treatment with other antianginal drugs (except other calcium antagonists) was permitted throughout the study. The baseline blood pressures were 166/93 and 160/91 mm Hg for the amlodipine group and diltiazem groups, respectively. Amlodipine (mean final daily dose of 9.25 mg) reduced blood pressure by - 27/-11 mm Hg compared with a reduction of - 17/-8 mm Hg for diltiazem (mean final daily dose of 180 mg), with no significant effects on heart rate. A significantly greater reduction in the mean rate-pressure product was observed after amlodipine (-20.8%) when compared with diltiazem (-13.1%) (p < 0.05). Amlodipine reduced the mean weekly angina attacks to zero after 6 weeks of treatment (baseline of 3.4 attacks/week) compared with a reduction from 3.3 to 0.35 attacks/week after 10 weeks of treatment with diltiazem. The amlodipine group had a reduction in mean nitroglycerin consumption from baseline of 1.1 mg/week to zero by week 6, whereas the diltiazem group had reduced mean weekly intake from 0.9 to 0.1 mg at the end of the study. The overall assessment of clinical efficacy was excellent for 100% of amlodipine patients compared with 40% of diltiazem patients. The high-density lipoprotein cholesterol/total cholesterol ratio increased by 15.8% with amlodipine compared to diltiazem, which produced a 4.5% decrease. Amlodipine decreased triglycerides by 7.1% compared to 4.5% with diltiazem. The incidence and severity of side effects was comparable for both treatments. Amlodipine once daily was effective and well tolerated in the treatment of patients with symptomatic myocardial ischemia and was comparable with diltiazem three times daily.

A group of 30 patients with II-III NYHA class cardiac insufficiency was treated with ibopamine in association with other drugs for a 6-month period. The patients were submitted to a 24-h ambulatory ECG Holter monitoring, chest X-ray, Doppler echocardiography in order to calculate total peripheral vascular resistance. Blood levels of aldosterone and renin-angiotensin activity in plasma were also measured, together with norepinephrine excretion. The measurements and recordings were performed in basal conditions before the trial, and were repeated after the first, second, third and sixth month. Laboratory tests were performed at the baseline and after 6 months. The results showed a significant decline in the number of ventricular and supraventricular ectopic beats after treatment. Heart rate did not change. Cardio-thoracic ratio decreased significantly along with peripheral vascular resistance. A very noticeable decline in all three neurohormonal parameters, i.e. norepinephrine excretion, blood level of aldosterone and renin activity in plasma was observed after 1 month's treatment, and this reduction was still present without any attenuation after 6 months. No significant changes were observed in routine laboratory tests.

Left ventricular (LV) performance was studied in young patients with severe chronic anemia due to beta-thalassemia major, intermedia, and in healthy control subjects. M-mode echocardiograms were recorded in each patient and semiautomatic computerized analysis of the tracings provided data relating to LV performance. Then a statistical analysis of the difference between each specific thalassemic group and the normal subjects was made using Student's t-test for unpaired data. The study showed that cardiac dysfunction is more serious in major than in intermediate beta thalassemia. A follow-up one year later showed a progressive deterioration of the cardiac indices, in spite of treatment with desferrioxamine. A handgrip test was performed in the follow-up study, which permitted us to distinguish different groups relative to the changes in LV performance indices. Our findings indicate that echocardiography provides a simple noninvasive means for assessing changes in the cardiac structure and function, which should also prove useful in the serial evaluation of patients at risk of developing myocardial iron deposition.

The discovery tha carnitine takes an active part in the transportation of long-chain acyl residues across the inner mitochondrial membrane dates back to 1958. It has been shown experimentally tha a reduction in myocardial carnitine content takes place after 15-30 min of ischemia. L-carnitine was administered orally in doses of 3 g/day for 30 days to 16 subjects with effort-induced angina and to 14 healthy subjects. A bicycle ergometer exercise test revealed a 1.5 mm (mean) depression of the ST-T segment in the angina subjects after pharmacological wash-out and a 1 mm depression in the same subjects after carnitine treatment. M-code echocardiography showed positive changes in a number of ventricular function parameters in the angina subjects and also, to a lesser extent, in the healthy controls.