Biomedical subjects
Publications and source records attributed to C Manca.
This report describes a case in which serial cross-sectional echocardiographic examinations allowed us to make the diagnosis and to follow anatomical evolution of pulmonary thromboemboli. Frequent (three times a day for seven days) echocardiographic surveillance of thromboemboli allowed us to assess the effectiveness of the therapeutic approach.
Steroid sex hormones, testosterone, progesterone and diethylstilbestrol, have been tested on the isolated rabbit heart. These hormones produced a negative inotropic effect (1-10 mumol/l) and an inhibitory effect on the vasopressin- or ergonovine-induced coronary spasm (0.1-10 mumol/l). Basal coronary tone was increased by testosterone and progesterone, while diethylstilbestrol induced a slight reduction of coronary perfusion pressure. The negative inotropic effect was reversed by calcium and isoprenaline, thus resembling the calcium entry blocker activity. The activation of myocardial and coronary contractility by the calcium agonist, Bay K 8644, was antagonized by all these hormones. These observations demonstrated an influence of steroid sex hormones with calcium fluxes in the isolated rabbit heart.
Intravenous flecainide (2 mg/Kg for 15 min) was used in 30 patients (18 men and 12 women aged 23 to 85 years: mean 62) with recent or paroxysmal atrial fibrillation: 5 patients returned to sinus rhythm during flecainide administration while other 23 patients did it not later than 2 hours. Treatment with intravenous flecainide proved to be safe without significant side effects. Further investigations are required to define the effects of flecainide in the treatment of atrial fibrillation; at the moment it must be admitted that flecainide acetate is a useful, safe, fast acting drug for the conversion of paroxysmal or recent atrial fibrillation to sinus rhythm.
The obstruction of the left ventricular tract outflow following mitral valve surgery, as a late complication, is rarely reported in the literature. The case of a 47-yr-old woman, who, after mitral valve surgery, developed dynamic left ventricular tract outflow obstruction four years later is reported. This alteration was detected by 2D echo-Doppler. The echocardiographic findings were: 1) Normal function of the mitral prosthesis. 2) An equal pressure-gradient of 44 mmHg at rest and of 75 mmHg after amyl nitrite at three examined levels: below, above and at the level of the aortic valve. 3) A hyper-echo image in the peri-annular region, probably representing fibrous degeneration around the valve ring, which was the likely cause of the obstruction. Th data were confirmed by cardiac catheterization. The echocardiographic technique appears to be a useful tool to detect and study this complication of mitral valve surgery.
This study was undertaken to determine the acute effects of nifedipine on left ventricular filling, examined by Doppler echocardiography in patients with arterial hypertension and normal left ventricular systolic function. Twenty-seven patients with mild to moderate systemic hypertension, and 18 normotensive subjects were studied. Pulsed Doppler, M-mode and B-mode measurements were performed before and 30 min after sublingual nifedipine administration (10 mg). Peak E, peak A, area A, area E, ratio area A/area E, E deceleration and E acceleration time were measured. Before administering nifedipine, some of these diastolic filling parameters were significantly different in the hypertensive patients as compared with normal subjects. After nifedipine, in patients with arterial hypertension, peak E and area E increased significantly (p less than 0.01), while ratio peak A/E and ratio area A/area E showed a significant decrease (p less than 0.001). No significant changes were observed in normal subjects. The result of this study demonstrates that the acute administration of nifedipine modifies transmitral flow velocity pattern in hypertensive patients, suggesting that the left ventricular filling abnormalities are in part dynamic and reversible.
The effects of digitalis on the left ventricular diastolic phase are very scant. In order to gain a better insight into this problem, we measured the hemodynamic effects of an intravenous injection of K-strophantidin (0.005 mg/kg in a bolus given within 5-10 min) during the diastolic phase in 9 normal male subjects and in 9 male patients with coronary artery disease (CAD), maintaining a normal overall ejection fraction despite of the presence of some hypokinetic segments. Administration of K-strophantidin decreased significantly in normal controls the left ventricular volumes at 1/3, 1/2, 2/3 of the diastolic phase, whereas it did not produce significant change in CAD patients. Digitalis decreased the first and increased the second filling peak of the volumetric variable dV/dt in the normal controls, but not in the CAD patients. In the latter group the 2 peaks before digitalis administration were similar. The effects of digitalis on the dV/dt measured during the second filling peak were significantly different in the 2 groups. The increments of pressure in middle and end diastole in CAD patients were significantly greater than those observed in normal controls. Results of the present study suggest that digitalis has a negative influence on the left ventricular filling phase both in normal and CAD subjects. In fact digitalis modifies in normals the pattern of the left ventricular filling phase whereas it induces an untoward increase in the middle and end diastolic pressure in CAD patients.
Beta-adrenergic agonists can progressively lose their efficacy during chronic therapy in patients with heart failure. Ibopamine is a new dopamine derivative, active on dopaminergic and beta-adrenergic receptors, whose hemodynamic activity has been acutely demonstrated. To assess whether any attenuation of its efficacy occurs, the variations of the cardiac output induced during chronic therapy were monitored by impedance cardiography in 15 patients with dilated cardiomyopathy who showed a significant increase of the cardiac output (20.7 +/- 10.0%) after acute ibopamine administration. The efficacy of ibopamine was also assessed after 6 and 12 months of therapy by echocardiography, exercise testing, and 24-hour dynamic electrocardiogram (EKG) monitoring. The cardiac output response to ibopamine did not show any significant attenuation (range 15% to 19%) in the evaluations at 1, 2, 3, 4, 8, and 12 months of therapy. No significant change, was noted, after 6 and 12 months, in the exercise capacity (505 vs. 602 and 604 seconds) and the fractional shortening (16.2 vs. 18.3 and 18.5) without any change of the diastolic diameter. Ventricular arrhythmias were significantly reduced after 6, but not 12, months of therapy. No significant change in the New York Association (NYHA) functional class was noted at 6 and 12 months of therapy (2.4 +/- 5 vs. 2.3 +/- 7 and 2.4 +/-0.6, respectively). Our results show that ibopamine can maintain its hemodynamic activity even during chronic therapy.
The metabolic effects of calcium channels blockers have already been studied both in normal and diabetic humans and results were quite controversial, depending on the drug used, the dose administered, and the type of patient. Little information exists on the use of Ca2+ antagonists in obese people, even if these persons are a population risk group for developing diseases in which these drugs may be requested for treatment. Thus, we evaluated, in obese humans, the metabolic effects of two Ca2+ antagonist drugs recently made commercially available to treat diseases such as hypertension and ischemic heart disease: nicardipine and diltiazem. Sixteen obese subjects were submitted to an intravenous glucose tolerance test (0.33 g/kg) (IVGTT) and an arginine test tolerance (30 g in 30 minutes) (ATT) before and after a week of oral treatment with nicardipine (60 mg/day) or diltiazem (360 mg/day). Plasma values of glucose, insulin, and C-peptide during IVGTT, and of glucose, insulin and glucagon during ATT did not show any modification during treatment with either drug. Thus the Ca2+ antagonists, nicardipine and diltiazem, at therapeutic doses in obese subjects do not significantly affect glucose tolerance or insulin and glucagon release.
Quantitative data on the normal variability of body surface maps (BSM) are scarce in the literature. This is one of the reasons why BSM are not yet widely used in clinical practice despite their superior information contents. In this study we determined the average value and variability of a number of parameters derived from BSM in a group of 36 normal adult males, ages 22 to 60. Forty to 60 homogeneous beats were averaged for each subject. This enabled us to extend our study to the low voltage intervals (P,PQ,ST,U) which encompass more than 60% of the entire P-U duration and to contribute new data to controversial issues, such as the presence of two simultaneous maxima during atrial excitation. The following parameters were measured: a) the coordinates of the absolute potential maximum and minimum on the chest surface during the entire cardiac cycle; b) the time course of four voltage-related functions, namely: highest instantaneous potential value on the chest surface, lowest (most negative) potential, highest potential difference, and surface integral of the absolute value of the potential function. In recent studies these parameters were shown to be of considerable value in discriminating normal subjects from different categories of cardiac patients.
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We have evaluated the effects of nifedipine and verapamil on rate of left ventricular relaxation in 26 patients having coronary arterial disease with normal ejection fraction and normal left ventricular contractility. None of the patients had myocardial infarction. All patients showed normal contractile indices and abnormally high values of T constant, neg, dP/dt and left ventricular protodiastolic pressure, suggesting an impairment of left ventricular relaxation. Nifedipine, injected intravenously (15 micrograms/kg) in 14 patients induced a significant reduction of afterload parameters and an increase of contractility. Nifedipine also improved left ventricular relaxation, as it induced a reduction of the T constant from 42 +/- 2 msec to 33 +/- 2 msec (P less than 0.01). It induced a tendency to a reduction of negative dP/dt and protodiastolic pressure without reaching statistical significance. Verapamil, injected intravenously in the remaining 12 patients (0.1 mg/kg as a bolus followed by chronic infusion of 0.005 mg/kg/min for 3 min) induced a reduction of the T constant from 43 +/- 10 to 37 +/- 6 msec (P less than 0.01). It reduced the negativity of dP/dt from 2302 +/- 273 to 2021 +/- 252 mm Hg/sec (P less than 0.05) and of left ventricular protodiastolic pressure from 3.2 +/- 1.4 to 1.5 +/- 1.1 mm Hg (P less than 0.01). Verapamil, like nifedipine, reduced the afterload parameters although to a lesser extent. It did not substantially affect the left ventricular contractility. These data suggest that abnormalities of left ventricular relaxation may precede changes in systolic function and that nifedipine and verapamil favourably modify the indices of left ventricular diastolic function in patients with coronary arterial disease.
We tested the response of plasma atrial natriuretic peptide (ANP) levels to the following physiological stimuli: postural changes; head-out water immersion; and physical exercise. Plasma ANP (p-ANP) levels were assessed by a specific, sensitive radio-immunoassay. Plasma ANP rose significantly when posture shifted from upright to recumbent for 1 h, but fell again to basal values after 10 min standing. Circadian variations did not affect the posture study. Head-out water immersion produced a prompt and remarkable (sevenfold) increase in p-ANP, with a plateau reached after 1 h and held until the end of the experiment (2 h). Plasma ANP levels were measured in 10 normal subjects performing supine treadmill exercise at 50% of maximum aerobic capacity for 30 min. Plasma ANP rose from baseline supine values after 15 min exercise, and remained elevated during the following 15 min exercise. During the recovery phase ANP showed a trend towards baseline values, with a 38% decrease attained after 30 min. We propose that the above tests could be used as ANP-stimulating manoeuvres in physiological and clinical conditions in man.
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We have studied the effects of 17 beta-estradiol on the left ventricular pressure and on the coronary perfusion pressure in isolated rabbit heart, in order to evaluate the action of this hormone on the myocardial contractility and on the coronary resistances. 17 beta-Estradiol has induced a negative inotropic effect starting from a concentration of 10(-6) M and a vasodilation starting from 10(-7) M when administered on a vasopressin-induced coronary spasm. These effects are not related to sex or to alpha-, beta-adrenergic, histaminergic, anaesthetic-like mechanisms, but seem to interfere with calcium transport.
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