Protective effect of nisoldipine on dipyridamole-induced myocardial ischemia: correlation with exercise electrocardiography.

BACKGROUND: Nisoldipine, a dihydropyridine calcium channel blocker with strong coronary dilatative action, is commonly used in the treatment of myocardial ischaemia; its beneficial effect on effort angina has been demonstrated by several previous reports. Infusion of dipyridamole in doses sufficient to provoke myocardial ischaemia in patients with significant coronary artery disease is used safely in imaging studies for diagnostic purposes. OBJECTIVE: To evaluate the potential effect of nisoldipine on dipyridamole-induced ischaemia and to compare the results with the effect of nisoldipine on exercise-induced ischaemia. METHOD: Twelve patients (10 men and two women, mean age 62 +/- 8 years) with significant coronary artery disease (at least 70% lumen reduction in at least one major coronary vessel) were selected for inclusion in the study. In accordance with the inclusion criteria, the patients exhibited an ischaemic diagnostic response to a multistage exercise electrocardiography stress test (> 0.15 mV ST segment depression compared with the resting electrocardiographic tracing) and to a dipyridamole-echocardiography test (transient left ventricular dyssynergy of contraction during infusion of dipyridamole up to 0.84 mg/kg over 10 min), after 3 days' cessation of antianginal treatment. After treatment with oral nisoldipine (10 mg twice daily) was introduced, the patients repeated the two tests, within 18 days of the first evaluation. RESULTS: The dipyridamole-echocardiography test was positive for ischaemia in 12 patients who were not receiving nisoldipine and in eight patients who were receiving the drug (100% and 67% respectively, P < 0.05). In the eight patients who gave positive dipyridamole-echocardiography tests both with and without treatment, dipyridamole time (time to onset of dyssynergy during the test) increased from 7.9 +/- 2.9 min to 10.2 +/- 3.1 min (P < 0.01). In these patients, no significant changes were observed, at ischaemia, in the severity and extent of induced dyssynergy, evaluated as wall motion score index (each of 16 left ventricular segments scored from 1 = normal to 4 = dyskinetic) after treatment (score variations from baseline to ischaemia: 0.20 +/- 0.11 without nisoldipine and 0.16 +/- 0.06 with nisoldipine; NS). Variations in dipyridamole time (arbitrarily considered to be 15 min in the negative dipyridamole-echocardiography test) were significantly correlated with variations in exercise time (duration of exercise to exhaustion or diagnostic positive response on the electrocardiogram): r = 0.75 (P < 0.01). No significant differences were recorded in rate-pressure product (beats/min x mmHg x 100) at peak ischaemia between patients who were or were not receiving nisoldipine, during either the exercise electrocardiography stress test (233 +/- 36 with nisoldipine and 244 +/- 39 without nisoldipine; NS) or the dipyridamole-echocardiography test (147 +/- 21 with nisoldipine and 133 +/- 30 without nisoldipine; NS). CONCLUSION: Nisoldipine treatment can protect from dipyridamole-induced ischaemia, being associated with a longer stress time, and completely preventing the development of ischaemia in some patients. The therapy-induced changes in ischaemic threshold during the dipyridamole-echocardiography test correlate with variations in exercise tolerance.

Hyperkinetic ventricular arrhythmias in very elderly people with and without cardiac disease. Correlation with left ventricular echocardiographic parameters.

BACKGROUND: Morphological and functional changes induced by aging can hamper a clear distinction between pathological or paraphysiological phenomena in very old people. The incidence of hyperkinetic ventricular arrhythmias, for example, progressively increases in the elderly, even in the absence of overt cardiac disease. METHODS: One-hundred fifty-two clinically stable patients older than 80 years, submitted within 15 days to clinical evaluation, 24-hour continuous ambulatory ECG monitoring and echo Doppler examination, in the absence of antiarrhythmic treatment, were retrospectively selected in order to evaluate the incidence of ventricular arrhythmias, in patients with and without significant heart disease. The further aim of the study was to correlate the number of arrhythmias with left ventricular morphological and functional parameters, echocardiographically assessed. From the initial population, 80 patients (41 males, age 83 +/- 3 years) had significant heart disease (ischemic, hypertensive or valvular): Group I. Seventy-two patients (30 males, age 83 +/- 3 years) had no clinical or instrumental signs of heart disease: Group II. RESULTS: Considering echocardiographic data, Group I patients had a significantly higher left ventricular end-diastolic diameter (52 +/- 6 mm vs 47 +/- 4 mm, p < 0.01), lower ejection fraction (57 +/- 10% vs 64 +/- 6%, p < 0.01) and higher mass (275 +/- 84 g vs 208 +/- 46 g, p < 0.01), when compared with Group II. From ECG monitoring data, significant differences between the two groups were recorded in the incidence of premature ventricular beats per hour (79 +/- 163 vs 15 +/- 34, Group I vs Group II, p < 0.01) and presence of complex phenomena (couplets, triplets and runs: 51% vs 22%, p < 0.01). In old patients with documented cardiac disease a significant correlation was present between premature ventricular beats incidence and left ventricular end diastolic diameter (r = 0.39, p < 0.05) and left ventricular ejection fraction (r = 0.40, p < 0.05), while in patients without heart disease, no significant correlation was found between incidence of premature ventricular beats and echocardiographic morpho-functional parameters. CONCLUSIONS: In conclusion, hyperkinetic ventricular arrhythmias are globally frequent in old persons of very advanced age (more than 80 years), but, also in this subset, a significant distinction in terms of incidence and severity of arrhythmias is present between subjects with and without cardiac disease. A significant correlation between incidence of premature beats and non-invasive morpho-functional left ventricular parameters is present only for patients with overt heart disease.

[Left atrial myxoma evidenced by silent acute myocardial infarction]. / Myxoma atriale sinistro manifestatosi con infarto del miocardio acuto silente.

A 64-year-old female patient was in-hospital admitted due to a traumatic femoral fracture. A routinely performed ECG showed signs of anterior acute myocardial infarction, clinically silent, and pathological levels of myocardial serum enzyme were recorded. The echocardiographic-Doppler examination confirmed the LV dyssynergy of contraction and, unexpectedly, revealed a large peduncolated and mobile mass in left atrium, connected to the interatrial septum and prolapsing in left ventricle, referable to myxoma. In the clinical history of the patient, a previous cerebral transitory ischemic attack was present (probably due to myxomatous embolization), but no any other cardiovascular symptoms. The patient successfully underwent coronary angiography, which showed no coronary artery disease, and cardiac surgery for tumoral removal. On the basis of clinical and instrumental data, also acute myocardial infarction may be considered a very likely consequence of a intracoronary embolus. Systemic embolization from left atrial myxomas are frequent; however, the involvement of coronary tree, with clinical manifestations and diagnosis during life, is extremely rare. Complete lack of symptoms due to atrial myxoma and myocardial infarction, and the fortuitous diagnosis of both diseases are peculiar findings of the reported case. Many systemic embolizations from myxomas, although sources of tissue damages, may likely occur without symptoms and may be unrecognized during acute period.

[Propafenone and flecainide in the therapy of ventricular arrhythmias]. / Il propafenone e la flecainide nella terapia delle aritmie ventricolari.

Flecainide and propafenone are antiarrhythmic drugs of the class 1C (Vaughan and Williams) commonly used for ventricular arrhythmias. The purpose of the present study was to evaluate the efficacy of these drugs in 170 consecutive patients with ventricular arrhythmias who referred to our cardiological ambulatory. The study population was divided into two groups according to the absence (group A,82 patients) or presence of organic heart disease (group 1B: 51 patients with left ventricular ejection fraction (LVEF) >35%; group 2B: 37 patients with LVEF<35%). Ventricular arrhythmias were evaluated with a 48 hours Holter monitoring at baseline, and with a control 24 hours Holter monitoring at 15 days (for optimizing the dosage), at 5 months and at 10 months from the beginning of antiarrhythmic therapy. Patients of group A were randomly assigned to antiarrhythmic treatment (flecainide 150-300 mg/die or propafenone 450-900 mg/die). For patients of group B, such choice was leaded by the clinical and strumental data (32 patients were treated with flecainide, 56 patients with propafenone). In the 160 patients who ended the 10 months follow-up, we observed the following results: patients of group A showed a mean percentage reduction in incidence of premature ventricular complexes (PVC) after therapy in comparison to basal conditions of 93% and 89% with flecainide and propafenone, respectively, after a treatment of 5 months (p < 0.001); after 10 months mean percentage reduction of PVC was 91% with each drug (p = n.s.); complex ventricular events (CVE) were reduced of 90% and of 100% after 5 and 10 months, respectively, of treatment with flecainide and of 100% both after 5 and 10 months of treatment with propafenone (p = n.s.) -- patients of group 1B showed a mean percentage reduction of PVC of 87% and 84% after 5 and 10 months, respectiively, of treatment with propafenone (p = n.s.); after 5 months of therapy mean percentage CVE reduction was 66% with flecainide and 86% with propafenone (p < 0.001); after 10 months this mean reduction was 53% with flecainide and 73% with propafenone (p < 0.001). -- patients of group 2B showed a mean reduction of PVC of 59% and 58% after 5 and 10 months of therapy with flecainide, and of 65% and 67% after 5 and 10 months of therapy with propafenone (p = n.s.); CVE were reduced of 28% with flecainide and of 47% with propafenone after 5 months of treatment (p < 0.001) and of 36% with flecainide against 52% with propafenone after 10 months (p < 0.01). In the present study there was no significant difference between the two drugs in terms of tollerance and collateral effects (8% with flecainide vs 7%, with propafenone). Our results confirm the efficacy of the 1C class drugs in the treatment of "essential" ventricular arrhytmias. This efficacy appears reduced in non selected patients with organic heart disease. In these latter patients propafenone has shown more efficacy than flecainide in reducing CVE.

[Efficacy of ubidecarenone in the treatment of patients with cardiac insufficiency]. / Efficacia dell'ubidecarenone nel trattamento di pazienti affetti da insufficienza cardiaca.

In 11 patients suffering from medium to severe heart failure, we performed a clinical and instrumental study to evaluate the effectiveness of ubidecarenone (60 mg/die in a single oral dose), in addition to conventional treatment with digitalis and diuretics. After an 8-month follow-up in most patients we observed a significant improvement in clinical symptoms and in quality of life. Furthermore we were able to demonstrate a statistically significant decrease in left atrium dimensions (p less than 0.01), end-diastolic (p less than 0.01) and end-systolic (p less than 0.05) left ventricular diameters and a significative reduction in the distance of the septum from the e point of the mitral valve (p less than 0.05), expression of significant improvement of cardiac output.