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Biomedical subjects

M Marzilli

Publications and source records attributed to M Marzilli.

At least 73 records · Page 4Linked to original sources
PubMed1986

Dipyridamole-echocardiography test in patients with exercise-induced ST-segment elevation.

Fourteen consecutive patients with exercise-induced ST-segment elevation in the absence of previous infarction and basal left ventricular asynergy at rest performed a dipyridamole test (infusion of dipyridamole, 0.14 mg/kg/min intravenously for 4 minutes) during 12-lead electrocardiographic (ECG) and 2-dimensional echocardiographic monitoring. In 7 of the 14 patients, dipyridamole infusion consistently induced ST-segment elevation in the leads that showed ST elevation on effort; reversible asynergy (occurring in the region corresponding to the ECG leads with diagnostic changes) could always be documented by echocardiography. In 2 patients dipyridamole induced reversible asynergy in presence of ST-segment depression. In these 9 patients angiography invariably revealed a severe organic stenosis in the coronary artery feeding the region that became transiently asynergic after dipyridamole. In the other 5 patients (all of whom had either spontaneous or ergonovine-induced ST-segment elevation), the dipyridamole test yielded no significant echocardiographic or ECG change; coronary angiography showed absent (2 patients) or significant (3 patients) coronary artery disease. In conclusion, dipyridamole may induce transmural ischemia in humans, as detected by the electrical hallmark of ST elevation; this ECG pattern, in contrast to ST depression, reliably predicts the presence and site of transient regional asynergy. When dipyridamole induces ST-segment elevation, severe basal stenosis is invariably present in the coronary artery supplying the transiently asynergic myocardial region.

Adult↗
PubMed1986

Coronary extravascular compression influences systolic coronary blood flow.

The purpose of this study was to determine whether a relation exists between systolic coronary blood flow and systolic coronary extravascular compressive forces. Studies were performed in seven open-chest dogs in which the left anterior descending coronary artery was cannulated and perfused from the left carotid artery. Pressure within the left ventricular subepicardium, a measure of coronary extravascular compression in the subepicardium, was measured with a 1-mm-diameter catheter-tip micromanometer inserted directly into the myocardium in the region of perfusion. Systolic extravascular compressive forces were augmented by a local intracoronary injection of 1 microgram isoproterenol. Measurements were made in the presence of coronary vasomotor tone and were repeated following local maximal vasodilatation with adenosine. In the regulated coronary bed, systolic coronary flow decreased (18 +/- 4 vs -2 +/- 4 ml/min, P less than 0.01) as intramyocardial pressure increased (127 +/- 5 vs 222 +/- 12 mmHg, P less than 0.001). Similarly, in the maximally vasodilated coronary bed, systolic coronary flow decreased (103 +/- 16 vs 38 +/- 11 ml/min, P less than 0.001) as intramyocardial pressure increased (112 +/- 6 vs 204 +/- 16 mmHg, P less than 0.001). These observations indicate that an augmentation of coronary extravascular compressive forces during systole is accompanied by a diminution of systolic coronary flow irrespective of coronary vasomotor tone.

Animals↗
PubMed1986

Transient myocardial dysfunction during pharmacologic vasodilation as an index of reduced coronary reserve: a coronary hemodynamic and echocardiographic study.

Regional coronary flow reserve and regional myocardial contractility were evaluated in 29 patients after maximal pharmacologic coronary vasodilation (intravenous dipyridamole, 0.56 mg/kg body weight, administered over 4 minutes). Nineteen patients had a severe (80 to 99%) proximal and isolated stenosis of the left anterior descending coronary artery and 10 patients had normal coronary arteries; all had normal ventricular function under rest conditions. Myocardial contractility was assessed by means of continuous two-dimensional echocardiographic monitoring; coronary reserve was evaluated by coronary sinus thermodilution. After dipyridamole infusion, 9 of the 19 patients with left anterior descending artery stenosis had transient myocardial asynergy involving the septum or apex, or both (Group IA), whereas 10 patients showed no asynergy (Group IB). No impairment of contractility was observed in the 10 patients with normal coronary arteries (Group II). Coronary blood flow was measured under basal conditions and up to 10 minutes after the end of dipyridamole infusion. In patients in Group II, dipyridamole induced an increase in great cardiac vein flow of 167 +/- 68% (mean +/- SD). The 10 patients in Group IB showed a response comparable with that of the control group (Group II) (136 +/- 45% increase in great cardiac vein flow; NS versus Group II), whereas the 9 patients in Group IA had an increase of 46 +/- 30% (p less than 0.01 versus both Group IB and Group II). No significant difference was found in the angiographic severity of the stenosis expressed in terms of minimal cross-sectional area (Group IA = 0.30 +/- 0.13 mm2, Group IB = 0.34 +/- 0.18 mm2; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study.

The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Relation of intramyocardial pressure to coronary pressure at zero flow.

The purpose of this study was to determine the extent to which coronary pressure at zero coronary flow (Pf=0) may relate to extravascular compressive forces determined by direct measurements of left ventricular intramyocardial pressure. Studies were performed in nine open-chest anaesthetized dogs in which the anterior descending coronary artery was cannulated and perfused from the carotid artery. Coronary pressure was measured at the tip of the cannula. Intramyocardial pressure was measured with a 1 mm diameter micromanometer inserted directly into the subepicardium. The atrioventricular node was obliterated by cautery and the heart was electrically paced. Long diastolic pauses, sufficient to allow coronary flow to reach zero, were produced by the cessation of electrical pacing. In the autoregulated coronary bed, Pf=0, 47 mmHg (s.e.m. = 9), exceeded subepicardial pressure at zero flow, 23 mmHg (s.e.m. = 2; P less than 0.001). During maximal vasodilatation with adenosine, Pf=0, 16 mmHg (s.e.m. = 11), was not significantly different from subepicardial pressure at zero flow, 21 mmHg (s.e.m. = 4). These observations indicate that, in addition to coronary vasomotor tone, diastolic myocardial tissue pressure is important in the genesis of Pf=0.

Animals↗
PubMed1985

"Ischemia at a distance" during intermittent coronary artery occlusion: a coronary anatomic explanation.

The mechanism of electrocardiographic ST segment changes during acute coronary occlusion was evaluated in 28 consecutive patients with single vessel coronary artery disease undergoing coronary angioplasty. Patients were continuously monitored with a six lead electrocardiogram. Twenty-three patients showed ST changes in the primary zone of occlusion, and 13 of these had additional ST changes in a remote zone. Ten of these 13 had unusually extensive arteries supplying the remote zone. The balloon occluded two adjacent normal arteries in two patients, and no coronary anatomic explanation was evident in one patient. Ten patients with striking primary zone ST changes showed no remote change. Seven had nonextensive primary zone arteries, and three others had abundant collateral vessels. Five patients showed no electrocardiographic changes in primary or remote zones. Four had collateral vessels, and one had left ventricular hypertrophy on the baseline electrocardiogram. It was concluded that remote electrocardiographic changes are probably due to occlusion of unusually extensive coronary arteries and are not simply reciprocal.

Angioplasty, Balloon↗
PubMed1985

Intramyocardial pressure and coronary extravascular resistance.

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastolic, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blow flow.

Animals↗
PubMed1985

Effect of dilazep on coronary and systemic circulations.

In order to assess the effects of dilazep on central hemodynamics and regional flows, 0.2 mg/kg of the drug were administered intravenously to 6 open-chest anesthetized dogs. Hemodynamic and flow measurements were performed under control conditions, and approximately 5, 10 and 25 min after treatment. Dilazep caused a marked and sustained reduction of coronary resistance and increased coronary blood flow. Flow increased uniformly in the subendocardial and subepicardial layers of the left ventricle so that no significant change occurred in the endo/epi flow ratio. Dilazep caused a significant reduction of total systemic resistance and aortic pressure, however flow to the liver, kidney and spleen was not reduced. We conclude that dilazep exerts a dilating action on the coronary and systemic arterial beds and increases uniformly regional myocardial blood flow. Dilazep does not alter the transmural distribution of coronary blood flow and does not impair kidney, liver and spleen perfusion.

Animals↗
PubMed1985

Assessment of papillary muscle function in the intact heart.

A technique is described to localize the anterolateral papillary muscle and to assess its performance in vivo. Using this technique, we measured sequentially the pressure generated within the anterolateral papillary muscle and its changes in length during the cardiac cycle in eight open-chest anesthetized dogs. Pressure within the anterolateral papillary muscle was measured with a 1.6 mm diameter micromanometer probe. Its dimensional changes were measured with ultrasonic crystals. Pressure within the anterolateral papillary muscle exceeded left ventricular pressure throughout the entire cardiac cycle. A difference of 200 +/- 23 mm Hg was present between systolic pressure in the anterolateral papillary muscle and left ventricular systolic pressure (348 +/- 25 vs 149 +/- 6 mm Hg) (p less than .001). Shortening of the anterolateral papillary muscle began 25 +/- 2 msec after the upstroke of the aortic pressure, continued throughout isovolumic relaxation, and was maximal 68 +/- 5 msec after the apex of the aortic incisura. The extent and velocity of shortening of the anterolateral papillary muscle were maximal when pressure within the muscle was lowest. This temporal dissociation between pressure and dimensional changes of the anterolateral papillary muscle appeared to result from cyclic changes of loading imposed on the muscle.

Animals↗