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Biomedical subjects

M Marzilli

Publications and source records attributed to M Marzilli.

At least 91 records · Page 5Linked to original sources
PubMed1984

Effects of dilazep on coronary and systemic hemodynamics in humans.

The cardiovascular effects of dilazep, a new antianginal drug, were investigated in 18 patients, who underwent cardiac catheterization and coronary angiography for the evaluation of chest pain. Dilazep, 0.2 mg/kg, was injected intravenously over 1 to 2 minutes. The changes induced by dilazep in coronary tone were assessed by quantitative angiography in four patients, changes in systemic and coronary hemodynamics and blood gases in eight patients, and changes in systemic and pulmonary hemodynamics and blood gases in six. In 6 of the 18 patients the effects on hemoglobin-O2 oxygen binding were also investigated. Following dilazep administration, we observed a marked reduction of coronary resistance (six patients) (0.5 vs 1.0 mm Hg X min X ml-1, p less than 0.01) and of aortic-coronary sinus oxygen difference (seven patients) (4.6 vs 12.3 vol%, p less than 0.01), and a 23% increase in coronary diameter (four patients) (p less than 0.001). Total systemic resistance was also reduced by dilazep (six patients). Conversely, only minimal or insignificant changes were observed in heart rate (14 patients), aortic pressure (14 patients), total pulmonary resistance (six patients), myocardial oxygen consumption (six patients), double product (14 patients), blood gases (seven patients), and hemoglobin-oxygen affinity (six patients). We conclude that dilazep exerts a powerful dilating action on coronary vasculature without appreciable increase of myocardial oxygen consumption and cardiac work simultaneously with a reduction of peripheral resistance.

Adult↗
PubMed1984

Regional myocardial performance before, during and after coronary occlusion.

The effects of transient coronary occlusion upon segment length and intramyocardial pressure were studied in seven open-chest dogs. The subendocardial and subepicardial layers in the territory of the left anterior descending coronary artery were instrumented with pairs of ultrasonic crystals and miniature pressure probes. During coronary occlusion, systolic subendocardial pressure decreased from 194 +/- 11 to 141 +/- 12 mmHg (p 0.001) and systolic subepicardial pressure from 82 +/- 7 to 62 +/- 12(p 0.05). Systolic shortening was abolished in both layers. During reperfusion, systolic subendocardial pressure reached 242 +/- 22 mmHg (p 0.05) and systolic subepicardial pressure 100 +/- 10 mmHg (p 0.05). Early during reperfusion a transient overshooting was also observed in subendocardial and subepicardial systolic shortening. The observations of this study are consistent with the hypothesis that unrestricted reperfusion is associated with an overshooting in regional myocardial contractile performance.

Animals↗
PubMed1984

Regional myocardial systolic function. Effects of coronary occlusion and reperfusion.

Intramyocardial pressure and segment length were measured during control conditions, during 30 sec coronary artery occlusion, and during reperfusion in the subendocardial (ENDO) and in the subepicardial (EPI) layers of the left ventricular wall, in 9 open-chest dogs. Under control conditions systolic subendocardial pressure, 179 +/- 11 mmHg, exceeded subepicardial pressure, 97 +/- 9 mmHg (P less than .001); the maximal rate of change of pressure in the subendocardium, 2231 +/- 170 mmHg/sec, was greater than in the subepicardium, 960 +/- 125 mmHg/sec, (P less than .001). Subendocardial systolic shortening, 23 +/- 2% was greater than subepicardial systolic shortening 16 +/- 1% (P less than .001). The maximal rate of systolic shortening in the subendocardium, 32 +/- 5 mm/sec, was also higher than in the subepicardial, 14 +/- 1 mm/sec (P less than .001). When the left anterior descending coronary artery was closed, subendocardial and subepicardial systolic pressures decreased immediately; conversely, appreciable changes in segment length were delayed 10-12 heart beats. After 30 sec of coronary occlusion a 35% reduction was observed in subendocardial and subepicardial systolic pressures, and systolic lengthening occurred. During reperfusion systolic shortening showed a brief overshooting and was back to control after 10 +/- 2 sec in subepicardium and 13 +/- 2 sec in subendocardium. Systolic intramyocardial pressure recovered in 14 +/- 3 sec in EPI and 18 +/- 2 sec in ENDO and subsequently rose above control level. Peak rebound occurred after 50-75 sec of reperfusion and was 27% higher than control in subendocardium and 20% in subepicardium. In 5 dogs the effects of coronary occlusions lasting 5, 15, 30, 45 and 60 sec were investigated. A progressive increase in ischemic depression and reperfusion rebound in subendocardial and subepicardial pressures was observed. These data show that subendocardial and subepicardial are both functionally depressed by coronary occlusion and that subendocardial and subepicardial both contribute to reperfusion hyperkinesis. Systolic intramyocardial pressures persist when shortening is abolished. Ischemic depression and reperfusion rebound of systolic intramyocardial pressures are affected by duration of coronary occlusion.

Animals↗
PubMed1983

Coronary vasodilation by nitrates is not mediated by the prostaglandin system: an angiographic and hemodynamic study.

The possible role of prostaglandins in mediating coronary vasodilation by nitrates was investigated in 13 patients. In nine patients (Group 1), the effects of ISDN on coronary-artery diameter and (in four of the nine) coronary sinus flow before and after administration of ASA were compared. In four additional patients (Group 2) the first ISDN administration was omitted in order to investigate the effect of ASA on resting coronary artery tone. Dosages used were 3 mg intracoronary ISDN and 1.0 g intravenous and 100 mg intracoronary ASA. Coronary artery diameter was analyzed by means of quantitative magnification coronary angiography. Coronary sinus flow was investigated by means of coronary sinus thermodilution. ASA was not able to induce significant changes in coronary artery diameter when injected before administration of ISDN or to prevent ISDN-induced vasodilation. At the coronary resistance level, ASA was not able to prevent the relative vasodilation induced by ISDN. It is concluded that coronary vasodilation by nitrates is not mediated by the prostaglandin system.

Aspirin↗
PubMed1981

The relative role of subendocardium and subepicardium in left ventricular mechanics.

The purpose of this study was to determine whether differences of wall thickening and fiber shortening exist between the deep and superficial layers of the left ventricular (LV) wall during systole. By use of ultrasonic crystals, wall thickness and segment-length changes were studied in seven dogs, and changes of the internal and external diameter of the LV were studied in five dogs. Radiopaque markers were used in conjunction with ventriculograms to determine the changes of the internal and external volume of the LV in five additional dogs. The subendocardial portion of the LV wall accounted for 83% of wall thickening during diastole. Segments of the subendocardium shortened 18% during systole, whereas segments of the subepicardium shortened only 10%. A 22% reduction of the internal LV diameter occurred in comparison to only a 6% reduction of the external diameter during systole. Similar observations were made in relation to LV internal and external volumes. These results indicate that the subendocardium undergoes greater dimensional changes (both thickening and shortening) during systole than does the subepicardium.

Animals↗
PubMed1981

[Selective vasodilatation of the subepicardial coronary vasculature induced by carbochromen (author's transl)].

The effect of carbochromen on total and regional coronary blood flow was investigated in 6 anesthetized open-chest dogs. Total and regional myocardial blood flow was measured by radioactive microspheres, using the reference sample method. Left circumflex coronary flow was monitored by an electromagnetic flowmeter. In 4 dogs (Group 1) carbochromen was injected intravenously; in 2 dogs (Group 2) it was infused directly in the circumflex coronary artery. No significant changes in heart rate, left atrial left ventricular and aortic pressures were observed following carbochromen administration in both Groups. Left circumflex coronary blood flow progressively increased and a level slightly higher than peak reactive hyperemia was reached in both Groups. Regional myocardial blood flow measurements in Group 1 showed that the inner third of the left ventricular wall (ENDO) increased 2.7 times relative to control, the middle layer increased 3.4 times relative to control and the external third 4.5 times relative to control. A similar pattern was observed after intracoronary administration of carbochromen (Group 2). The ENDO/EPI flow ratio dropped from 0.98 +/- 0.16 to 0.58 +/- 0.18 in Group 1 and from 1.03 and 1.20 to 0.71 and 0.53 respectively in the two experiments of Group 2. Replacement of carbochromen with adenosine infusion in Group 2 produced a further increase in flow, mainly in the subendocardium resulting in ENDO/EPI flow ratio close to unity. These data demonstrate that the powerful coronary vasodilatory effect of carbochromen is not uniform being vasodilation more prominent in the vasculature of the external third of the left ventricular wall as compared to the inner third. Consequently a major redistribution of coronary blood flow, favouring the external layers of the left ventricle, results from carbochromen administration. This effect distinguishes carbochromen from other vasodilating stimuli than elicit a uniform response in the coronary vasculature and do not affect the ENDO/EPI ratio, including transient ischemia, adenosine, and dipyridamole.

Animals↗
PubMed1980

Intracardiac phonocardiography in experimental left ventricular cavity obliteration: potential clinical applicability for the distinction of obliterating left ventricle from hypertrophic obstructive cardiomyopathy.

Intracardiac sound was measured in six dogs, four with left ventricular cavity obliteration induced by isoproterenol, and two with catheter entrapment. In left ventricular cavity obliteration, no murmur occurred within the left ventricle. Whenever a systolic murmur occurred, it was distal to the aortic valve. In entrapment, no murmur occurred within the left ventricle or distal to the aortic valve. Previous studies in patients with hypertrophic obstructive cardiomyopathy showed that the systolic murmur was of greatest intensity within the left ventricular outflow tract. Therefore, intracardiac phonocardiography may assist in differentiating these conditions which produce an intraventricular pressure gradient.

Animals↗
PubMed1980

Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis: a hypothetical pathogenesis.

This study explores the relation between coronary arterial spasm and the development of coronary atherosclerosis. The clinical history and coronary angiographic and electrocardiographic data in 212 consecutive patients with ischemic heart disease were correlated. These patients were classified into four groups: Group 1, patients without angiographic evidence of atherosclerosis; Group 2, patients with single vessel disease; Group 3, patients with double vessel disease; and Group 4, patients with significant narrowing of major coronary arteries. Although spontaneous angina occurred in all four groups, it was more common (55 percent) in the patients in Group 1, who were predominantly female and young. Spontaneous angina was confirmed in Group 1 with several techniques, including thallium-201 scintigraphy, ergonovine administration and electrocardiography during attacks of pain. Prior myocardial infarction was present with similar frequency in all four groups. A patient is discussed whose spontaneously occurring coronary arterial spasm later progressed to fixed arteriosclerotic narrowing requiring coronary bypass surgery. These observations and a review of the literature lend support to the hypothesis that coronary arterial spasm can be a possible antecedent leading to the later development of fixed atherosclerotic coronary arterial obstruction.

Adult↗
PubMed1980

Role of the papillary muscle in opening and closure of the mitral valve.

Dimensional changes of the left ventricular anterolateral papillary muscle of six open-chest dogs were measured continuously throughout the cardiac cycle in order to evaluate the role of the papillary muscle in opening and closing of the mitral valve. Dimensional changes were measured with ultrasonic dimension gauges. Maximal shortening and maximal elongation of the papillary muscle followed maximal shortening and elongation of a segment of the free wall of the left ventricle by 65 +/- 6 (SE) ms. Maximal elongation of the papillary muscle occurred 25 +/- 2 ms after the onset of ejection. Maximal shortening of the papillary muscle occurred 68 +/- 5 ms after the aortic incisura and 10 +/- 2 ms after the crossover of left ventricular and left atrial pressure. The papillary muscle shortened 14 +/- 4%. The percentage of papillary muscle shortening that occurred after the aortic incisura was 39 +/- 7%, and the percentage of shortening that occurred after the crossover of left ventricular and left atrial pressure was 3 +/- 1%. The observed shortening of the papillary muscle throughout left ventricular isovolumic relaxation suggests that the papillary muscle may have a role in opening the mitral valve. Conversely, elongation of the papillary muscle in the late portion of diastole appears necessary to permit proper closure of the mitral valve leaflets.

Animals↗
PubMed1980

Comparison of the distribution of intramyocardial pressure across the canine left ventricular wall in the beating heart during diastole and in the arrested heart. Evidence of epicardial muscle tone during diastole.

Computations of compliance of the left ventricle (LV) during diastole assume passive tissue characteristics. To evaluate this assumption, we measured diastolic LV intramyocardial pressure simultaneously in the subepicardium and subendocardium in 18 open-chest dogs, using 1-mm in diameter micromanometers. Subepicardial pressure, 26 +/- 1 mm Hg (mean +/- SEM) exceeded subendocardial pressure, 14 +/- 1 mm Hg (P less than 0.001), and it exceeded left ventricular end-diastolic pressure (LVEDP) (9 +/- 1 mm Hg) (P less than 0.001). After an infusion of dextran-40 (10 dogs), subepicardial diastolic pressure increased to 42 +/- 4 mm Hg which was higher than diastolic subendocardial pressure, 26 +/- 2 mm Hg (P less than 0.001) and LVEDP, 24 +/- 2 mm Hg (P less than 0.001). Following cardiac arrest (12 dogs) with the intramyocardial probes unchanged in position, LV intracavitary pressure, 9 +/- 1 mm Hg, and subendocardial pressure, 13 +/- 3 mm Hg, did not differ significantly from the pressures in the beating heart. Subepicardial pressure, 9 +/- 1 mm Hg, was lower than in the beating heart (P less than 0.001). Following distention of the arrested LV (12 dogs), subepicardial pressure, 31 +/- 7 mm Hg, was lower than both subendocardial pressure, 58 +/- 12 mm Hg (P less than 0.001) and LV intracavitary pressure, 54 +/- 11 mm Hg (P less than 0.001). These observations indicate that tone is maintained by the subepicardium during diastole. Furthermore, the LV wall does not appear to behave as a passive shell during ventricular filling.

Animals↗
PubMed1980

Mitral regurgitation in ventricular premature contractions. The role of the papillary muscle.

In view of the possibility that the mechanism of mitral regurgitation following premature ventricular contractions may contribute to the understanding of mitral regurgitation in clinically important causes of nonrheumatic mitral insufficiency, we studied 320 premature ventricular contractions in eight dogs. Since the papillary muscle is an important component of the mitral valvular complex, the extent and course of lengthening and shortening of the papillary muscle was investigated with ultrasonic crystals implanted within the anterolateral papillary muscle. Lengthening and shortening of a segment of the free wall of the left ventricle was measured simultaneously with identical crystals in three dogs. During sinus rhythm, lengthening of the papillary muscle always began well before the onset of isovolumic contraction of the left ventricle and continued throughout isovolumic contraction, indicating that lengthening occurred during closure of the mitral valve. When lengthening was prevented by premature ventricular contractions, left atrial v waves occurred. These observations indicate that lengthening of the papillary muscle during the latter part of diastole is required for proper closure of the mitral valve and that inadequate lengthening can result in mitral regurgitation.

Animals↗
PubMed1980

Supply-demand balance of subendocardial muscle: estimation from intramyocardial pressure.

The ratio of the dihastolic pressure-time index (DPTI) to the systolic pressure-time index (SPTI) has been used as a predictor of subendocardial ischemia. The DPTI is thought to reflect the blood supply to the subendocardium, and the SPTI is thought to reflect the metabolic needs. In this study, the supply-demand balance of subendocardial muscle was evaluated directly from the pressure measured within the subendocardium. The blood supply to the subendocardial muscle, estimated from the area between the aortic pressure and the subendocardial pressure in diastole (3,370 mm Hg sec min-1) (mean +/- SEM) was lower than the DPTI (4,060 mm Hg sec min-1) (p less than 0.01). The metabolic demand of the subendocardial muscle, estimated from the area included in the subendocardial pressure (4,820 mm Hg sec min-1) was higher than the SPTI (2,480 mm Hg sec min-1) (p less than 0.01). The supply-demand balance, directly estimated from subendocardial pressure, 0.7, was markedly lower than the simultaneous DPTI/SPTI ratio, 1.6. In view of the prominent differences between the supply-demand balance estimated by these two indices, the DPTI/SPTI ratio as a predictor of subendocardial ischemia may require further evaluation.

Animals↗