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Biomedical subjects

F Magrini

Publications and source records attributed to F Magrini.

At least 91 records · Page 5Linked to original sources
PubMed1971

Left ventricular performance and related haemodynamic changes in Prinzmetal's variant angina pectoris.

Attacks of Prinzmetal's variant form of angina pectoris are spontaneous, recur cyclically, and present unequivocal electrocardiographic alterations: they are ideal for a detailed haemodynamic study.Four patients with this form of angina were investigated. In each of them episodes occurred of electrocardiographic abnormalities either accompanied or unaccompanied by pain. During the same session, the cardiogram, heart rate, arterial pressure, and right atrial pressure were continuously recorded during periods ranging from 5 to 7 hours in each patient. Cardiac output was measured at selected times. Left ventricular ejection time, isovolumic contraction time, mean rate of isovolumic pressure development, and mean systolic ejection rate were also determined. In the 38 recorded anginal episodes, no circulatory change preceded the cardiographic modifications. From the onset of the electrocardiographic abnormalities to the beginning of their reversion, the following circulatory events were observed: (1) obvious reduction of cardiac output; (2) arterial hypotension; (3) lengthening of isovolumic contraction time and mean rate of isovolumic pressure development; (5) reduction of mean systolic ejection rate. It is concluded: (1) that no circulatory factor interfering with work or oxygen consumption of the heart is responsible for eliciting these anginal episodes; (2) that conspicuous left ventricular impairment occurs during the increasing and steady period of the electrocardiographic abnormalities. As the electrocardiogram started reverting to the pre-attack aspect, cardiac performance rapidly improved and, after a ;supernormal' phase, returned in about 2 minutes to basal levels. It is possible that this phase is dependent on a temporary sympathetic compensatory mechanism. No significant qualitative differences were detected between the circulatory pattern of various anginal episodes. The difference was mainly quantitative and the magnitude of the haemodynamic changes correlated well with the degree of the electrocardiographic abnormalities. Pain, when present, seemed just a concomitant symptom not significantly interfering with the circulatory changes associated with the episodes of this form of angina pectoris.

Angina Pectoris↗
PubMed1970

Continuous electrocardiographic recording in Prinzmetal's variant angina pectoris. A report of four cases.

Four patients with Prinzmetal's variant angina pectoris were subjected to continuous electrocardiographic recording. In three of them several episodes of ST segment elevation unaccompanied by pain were recorded. In one patient, identical electrocardiographic alterations were observed both in presence or in absence of pain, while in the others a good correlation was evident between pain and severity of the electrocardiographic abnormalities. In two patients transmural myocardial infarction complicated the course of the angina. In contrast to the classical findings, in these patients the attacks of chest pain did not cease after the infarction, but became more frequent and severe. The electrocardiographic alterations of the anginal episodes occurred in the same myocardial areas involved by the infarction, so that a reversible superposition of electrocardiographic signs of acute ischaemia on those of recent necrosis was observed. Continuous electrocardiographic recording provided the best means of investigation of these patients with the variant form of angina pectoris.

Adult↗
PubMedDate not supplied

Echocardiographic patterns of myocardial fibrosis in hypertensive patients: endomyocardial biopsy versus ultrasonic tissue characterization.

Echocardiographic image texture has been demonstrated to reflect the physical properties of the tissue under examination. To evaluate the role of collagen in determining the echo pattern of the left ventricular wall, we studied nine hypertensive patients with left ventricular hypertrophy (left ventricular mass index > 125 gm/m2) and biopsy-proven different degrees of myocardial fibrosis by analyzing the echocardiographic examinations performed before the biopsy. Myocardial tissue was sampled under fluoroscopy and two-dimensional echo guidance in the interventricular septum. Collagen volume fraction (CVF; normal range up to 2%) was taken as an index of fibrosis. The echo patterns were assessed by analyzing standard two-dimensional parasternal long-axis echocardiograms recorded on videotape. Images were color-coded at 256 levels (0 = yellow, 256 = black) and digitized off-line onto a personal computer. The region of analysis was set using a selection tool (20 x 10 mm) in the general area of septum where the specimen was taken. For each selection a color-level histogram, representing the frequency distribution, was derived with estimates of the average pixel intensity (mCS), skewness (SK), kurtosis (K), and the broad band (Bb) of the echoes about the distribution. Echo-derived parameters in each patient were compared with corresponding CVF values. CVF was out of range in all patients, ranging from 2.6% to 7.6% (mean 4.3% +/- 1.6%). No correlation was found between CVF and mCS, whereas a significant correlation was found at end diastole between CVF and the parameters describing histogram morphology, respectively, SK (r = 0.73), K (r = 0.69), Bb (r = 0.72). These findings for the first time demonstrate in vivo in hypertensive patients with left ventricular hypertrophy an agreement between echo amplitude and histologically assessed collagen volume. Thus in our studied patients collagen content appears to be the major determinant of regional echo intensity, its increase resulting in a significant and progressive wider asymmetrical left shift (yellow) of the color histogram.

Adult↗
PubMedDate not supplied

Long-term treatment of hyperkinetic heart syndrome with propranolol.

Twelve men suffering from the primary hyperkinetic heart syndrome (PHHS) displayed palpitation, rapid and forceful heart action, increased pulsations of the large arteries, cardiac systolic murmur, and the following circulatory values (averages): systolic arterial pressure (SAP) =154 mm Hg; heart rate (HR)=91 b/min; cardiac index (Ci) =5494 ml/min/m2; left ventricular mean systolic ejection rate index (SMEJR) =227 ml/min/m2; left ventricular mean pre-ejection delta P/delta t (delta P/delta t) = 1.32 mm Hg/msec. A two-year followup during which propranolol was administered (80-160 mg/day) revealed good subjective improvement and disappearance of signs of circulatory hyperkinesis. At the end of this period the hemodynamic functions were as follows: SAP=134; HR=69; Cl=3489; MSEJR=171; delta P/delta t=0.89. Substitution of placebo for the active drug caused prompt reappearance of symptoms of cardiac overactivity in each patient, and brought the circulatory functions back to these levels: SAP=157; HR=96; Cl=5530; MSEJR=245; delta P/delta t=1.33. These findings lend further credence to the concept that the PHHS is, indeed, a definable disease entity; they also document that propranolol ameliorates the symptoms of the disease but is ineffective for the underlying disorder.

Adolescent↗
PubMedDate not supplied

Cardiac performance and beta-adrenergic blockade in arterial hypertension.

The purpose of the study was to evaluate the functional changes which may occur in the human hypertensive heart following treatment with beta-blocking agents. In 54 primary hypertensive men investigated in the control state and after three weeks of treatment with propranolol (320 mg/day) it was seen that: (a) beta-adrenergic blockade depresses the pre-ejection, and probably the ejection left ventricular function; (b) the former effect is unrelated to changes in peripheral circulation, while the latter result may be either potentiated or overcome, depending on the direction to which treatment shifts the vascular resistance; (c) variations of impedance, rather than of blood pressure, influence the ejection left ventricular function; and (d) withdrawal of the adrenergic support to the heart, due to beta-blockade, is probably the primary factor responsible for the abnormal ventricular adaptation to an augmented impedance.

Blood Pressure↗