Federico Piscione

Impaired left ventricular filling dynamics during percutaneous transluminal angioplasty for coronary artery disease

The effects of brief periods of major coronary artery occlusion on global and regional peak left ventricular (LV) filling rates were studied during angioplasty in 10 patients. No patient had had a previous myocardial infarction. High-fidelity LV pressure and volume were determined by angiography before and 20 and 50 seconds after the onset of transluminal coronary occlusion and soon after the last balloon inflation. Segmental wall motion was analyzed frame by frame along 20 hemiaxes. Global peak filling rate decreased significantly both after 20 (29%, p less than 0.05) and 50 seconds (27%, p less than 0.05) from the onset of the occlusion. The term sigma delta t1 was defined as the sum of the absolute values of the time differences from the occurrence of global peak filling rate and the segmental peak filling rate in 20 segments. This variable increased significantly during both periods of transluminal occlusion (by 73% and by 72% [both p less than 0.005], respectively), indicating asynchrony in the occurrence of regional peak filling rate. Simultaneously, the sum of intervals between aortic valve closure (end systole) and occurrence of peak segmental shortening, sigma delta t2, measured in the 20 segments, increased by 63% after 20 seconds and by 87% after 50 seconds (both p less than 0.005), showing major asynchrony in segmental contraction. A significant negative correlation was found between global peak filling rate and both sigma delta t1 and sigma delta t2 (r = 0.64, p less than 0.001 and r = 0.70, p less than 0.0001, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional cardioprotection by subselective intracoronary nifedipine is not due to enhanced collateral flow during coronary angioplasty

Twelve patients with proximal stenosis of the left anterior descending artery, normal myocardial wall motion but without angiographically demonstrable collateral circulation, were studied during transluminal occlusion. Prior to the first transluminal occlusion before crossing the lesion with the balloon, patients were randomly given 0.2 mg nifedipine or its solvent in the left mainstem. The same dose was repeated via the balloon catheter, positioned across the lesion, immediately prior to the second transluminal occlusion. In all patients great cardiac venous flow and ST-elevation were monitored during and after each transluminal occlusion. The lactate extraction ratio A-GCV/A (A = arterial, GCV = great cardiac vein) was determined prior to the angioplasty procedure, 10-15 seconds after each transluminal occlusion and 10 minutes after the third transluminal occlusion. Great cardiac venous flow rose significantly to an average of 160% of basal flow when nifedipine was administered into the mainstem before the angioplasty procedure while its solvent had no effect. During each transluminal occlusion, great cardiac venous flow diminished on average by 30% in those who received nifedipine and by 28% in those who received only its solvent. This difference was statistically not significant. After angioplasty great cardiac venous flow was slightly, but not significantly, increased in both groups with respect to basal flow (104% resp. 120% of control). Patients who received nifedipine in the post-stenotic area just before the second transluminal occlusion, had significantly lower lactate production, measured immediately after the transluminal occlusion compared with the patients who received only its solvent (P less than 0.01). The ST-elevation during the second transluminal occlusion was significantly lower in the nifedipine group (0.1 mm in nifedipine group versus 1.4 mm in solvent group; P less than 0.05, unpaired t-test). Nifedipine given intracoronary in the post-stenotic area just before coronary angioplasty reduces lactate release and electrocardiographic signs of myocardial ischemic injury. This regional cardioprotective effect seems not due to an enhanced collateral flow, but to a regional cardioplegic effect, which precedes the ischemic event.

Ejection, Filling and Diastasis during Transluminal Occlusion in Man: Consideration on Global and Regional Left Ventricular Function

An extensive literature exists describing the acute changes in hemodynamics and left ventricular function following coronary occlusion in animals [1–4]. Much less, however, is known in man. Extrapolating results from animals to man is potentially difficult, since, in man preexisting atherosclerotic coronary disease and a unique distribution of collateral circulation [5–7] may influence findings.

Left ventricular function after oral milrinone in patients with congestive heart failure. A hemodynamic and angiographic study

The diastolic properties of the left ventricle (LV) are important determinants of cardiac function; alteration in diastolic function accounts for many of the clinical manifestations of congestive heart failure. Changes in myocardial relaxation and filling phases, changes in coronary blood flow, diastolic tone and ventricular shape all contribute to the abnormal diastolic compliance of the failing heart. To assess the short-term effects of a single oral dose (10 mg) of milrinone (M) on diastolic function, 14 patients (pts), mean age 59 ± 6 years, with severe congestive heart failure underwent this study. After baseline hemodynamic measurements, LV angiography with simultaneous recording of LV pressure (tip-manometry) and pressure-derived parameters was performed at paced heart rate (15 beats above spontaneous heart rate). After repeat baseline measurements, M was administered followed by LV pressure measurements at 10′ intervals to 50′ together with coronary blood flow measurement. Blood samples to determine the plasma concentration of M were withdrawn at the same intervals. Blood arterial and coronary sinus samples for catecholamine levels and oxygen saturations were withdrawn before and 50′ after M. LV angiography was repeated 60′ after M at matched atrial paced rates with simultaneous pressure recordings. During the first phase of the study, peak negative dP/dt progressively and significantly increased from 827 ± 209 to 904 ± 194mm Hg/sec (p < 0.01) whereas LV systolic pressure slightly decreased. The time constant of early relaxation, Tau1,(fit for the first 40 msec. after the occurrence of peak negative dP/dt), decreased progressively and significantly from 71 ± 17 to 58 ± 14 msec (p < 0.01). Minimal LV diastolic pressure and LV end-diastolic pressure (LVEDP) were significantly lowered after 50′ from 13 ± 4 to 10 ± 7 mm Hg (p < 0.05) and from 27 ± 7 to 20 ± 10 mm Hg (p < 0.01), respectively. Coronary blood flow rose progressively during the first 40′ but the increase failed to be significant at 50′. Coronary vascular resistance reciprocated these changes. Myocardial oxygen consumption remained unchanged over 50′. Noradrenaline, adrenaline and dopamine mean values also remained unchanged over 50′, thus demonstrating a lack of effect of M on the basal, elevated sympathetic tone. Mean plasma level of M rose progressively, achieving a therapeutic level after 30′. The analysis of LV volume, pressure and pressure-derived parameters during angiography showed an improved relaxation phase with an increase in peak filling rate from 290 ± 27 to 338 ± 55 ml sec. The constant of elastic chamber stiffness, measured by the simple elastic model, decreased but not significantly. Pressure-volume loops showed a downward shift in 10/14 pts, mainly because of a major reduction in LVEDP from 29 ± 10 to 20 ± 11 mm Hg (p < 0.001) while end-diastolic volume only slightly decreased.

Ejection filling and diastasis during transluminal occlusion in man

An extensive literature exists describing the acute changes in hemodynamics and left ventricular function following coronary occlusion in animals [1– 4]. Much less, however, is known in man. Extrapolating results from animals to man is potentially difficult, since, in man preexisting atherosclerotic coronary disease and a unique distribution of collateral circulation [5–7] may influence findings.

Effect of Coronary Occlusion During Percutaneous Transluminal Angioplasty on Systolic and Diastolic Left Ventricular Function, Coronary Hemodynamics, and Myocardial Energetic Metabolism

Until recently, the measurement in man of left ventricular geometry and hemodynamics and the assessment of alteration in myocardial metabolism early after an abrupt occlusion of a major coronary artery were not feasible. Percutaneous transluminal coronary angioplasty (PTCA), however, now provides a unique opportunity to study the time course of these variables during the transient interruption of coronary flow in the balloon occlusion sequence in patients with single-vessel disease and without angiographically demonstrable collateral circulation [1, 2].

Early changes in wall thickness and epicardial wall motion during percutaneous transluminal coronary angioplasty in man. Similarities with in vitro and in vivo model

Previously, our laboratory has reported the dynamic endocardial wall motion and myocardial wall thickness changes accompanying acute coronary occlusion in patients undergoing transluminal angioplasty (PTCA) [1, 2]. In these studies, the motion of the region of ischemic myocardium was characterized by the early appearance of a late systolic outward expansion followed by an early diastolic inward contraction. We refer to this biphasic motion as the “W” phenomenon due to its morphologic characteristics, transient duration, and frequency of appearance in studies of endocardial and wall thickness motion during regional ischemia. Similar types of wall motion abnormalities have been described with acute ischemia in animals [1, 2, 4] and in chronic ischemia in man [8, 9]. Since phasic wall motion can, in general, be encountered whenever spatial or temporal nonuniformities in regional contraction or relaxation in the left ventricle exist, the specific etiology of this pattern during acute ischemia is uncertain.

Myocardial release of hypoxanthine and lactate during coronary angioplasty

Until recently the assessment of alteration in myocardial metabolism in man early after an abrupt occlusion of a major coronary artery has not been feasible. Percutaneous transluminal coronary angioplasty (PTCA), however, now provides a unique opportunity to study the time course of these metabolic changes during the transient interruption of coronary flow by the balloon occlusion sequence in patients with single-vessel disease and without angiographically demonstrable collateral circulation [1, 2]. The need to detect any persisting metabolic or mechanical dysfunction becomes of even greater concern as the number of dilated vessels and the duration of balloon inflation tend to increase, thereby enhancing both the extent and the severity of ischemia. The risk exists that the damage induced by the intervention may exceed its benefit.

Early changes in wall thickness and epicardial wall motion during percutaneous transluminal coronary angioplasty in man

Previously, our laboratory has reported the dynamic endocardial wall motion and myocardial wall thickness changes accompanying acute coronary occlusion in patients undergoing transluminal angioplasty (PTCA) [1,2]. In these studies, the motion of the region of ischemic myocardium was characterized by the early appearance of a late systolic outward expansion followed by an early diastolic inward contraction. We refer to this biphasic motion as the ‘W’ phenomenon due to its morphologic characteristics, transient duration, and frequency of appearance in studies of endocardial and wall thickness motion during regional ischemia. Similar types of wall motion abnormalities have been described with acute ischemia in animals [1, 2, 4] and in chronic ischemia in man [8, 9]. Since phasic wall motion can, in general, be encountered whenever spatial or temporal nonuniformities in regional contraction or relaxation in the left ventricle exist, the specific etiology of this pattern during acute ischemia is uncertain.

Myocardial release of hypoxanthine and lactate during coronary angioplasty: A quickly reversible phenomenon, but for how long?

Until recently the assessment of alteration in myocardial metabolism in man early after an abrupt occlusion of a major coronary artery has not been feasible. Percutaneous transluminal coronary angioplasty (PTCA), however, now provides a unique opportunity to study the time course of these metabolic changes during the transient interruption of coronary flow by the balloon occlusion sequence in patients with single-vessel disease and without angiographically demonstrable collateral circulation [1, 2]. The need to detect any persisting metabolic or mechanical dysfunction becomes of even greater concern as the number of dilated vessels and the duration of balloon inflation tend to increase, thereby enhancing both the extent and the severity of ischemia. The risk exists that the damage induced by the intervention may exceed its benefit.