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Biomedical subjects

I Amende

Publications and source records attributed to I Amende.

At least 37 records · Page 2Linked to original sources
PubMed1990

Protective effects of pretreatment with intracoronary nifedipine on myocardial ischemia and dysfunction.

To assess whether pretreatment with intracoronary nifedipine protects the myocardium against acute ischemia induced by coronary occlusion, 18 patients were studied during coronary angioplasty of the left anterior coronary artery. After a control occlusion of 60 seconds, 0.1 mg nifedipine was injected and occlusion was repeated for 60 seconds. Before and during the occlusion period, pulmonary capillary pressure was measured and the intracoronary epicardial ECG was recorded. After intracoronary administration of nifedipine, the onset of the rise in diastolic filling pressure was delayed from 23 to 38 seconds (p less than 0.01) and the changes at 60 seconds of occlusion were reduced from 14 to 11 mmHg (p less than 0.05). Nifedipine delayed the appearance of ischemic ST-segment elevation in the intracoronary ECG from 11 to 21 seconds (p less than 0.01) and diminished the changes at 60 seconds of occlusion from 1.8 to 1.2 mV (p less than 0.05). These findings suggest that pretreatment with intracoronary nifedipine protects the myocardium against some of the mechanical and electrocardiographic consequences of regional ischemia during acute coronary occlusion.

Adult↗
PubMed1990

Role of thrombolysis and thrombin in patients with acute coronary occlusion during percutaneous transluminal coronary angioplasty.

In a series of 447 patients with single vessel angioplasty, 27 (6.0%) had acute thrombotic occlusion early after the procedure. They were treated with combined intracoronary (20 mg)/intravenous (50 mg) thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) and repeat mild balloon inflations. Reopening of the vessel was achieved in 22 patients (81.5%). Follow-up coronary angiography 24 to 36 h later revealed reocclusion in 12 patients (54.5%). Thrombin levels measured as thrombin-antithrombin-III complex in patients with successful thrombolysis and persistent patency decreased from 8.5 +/- 11.4 micrograms/liter at baseline to 3.5 +/- 1.4 micrograms/liter 120 min after the start of thrombolysis; these levels increased from 9.4 +/- 15.0 micrograms/liter at baseline to 15.7 +/- 13.5 micrograms/liter 120 min after the start of thrombolysis in the patients with unsuccessful thrombolysis or early reocclusion (p less than 0.05). When a borderline value for thrombin-antithrombin-III complex level of 6 micrograms/liter was selected to separate the two groups of patients, patients with an unfavorable clinical course were identified 120 min after the start of thrombolysis by levels greater than 6 micrograms/liter (sensitivity 100%, specificity 92.8%). Thus, after abrupt thrombotic vessel closure during coronary angioplasty, the short-term results of thrombolysis seem to be governed by the release of thrombin. In two thirds of patients, however, the thrombin release cannot be suppressed by concomitant aspirin and heparin therapy. Even after successful reopening of the vessel these patients should therefore undergo immediate aortocoronary bypass grafting.

Angioplasty, Balloon, Coronary↗
PubMed1990

Diastolic dysfunction during acute cardiac allograft rejection.

Left ventricular diastolic function was evaluated in 41 heart transplant patients during acute rejection by an analysis of echocardiograms and surgically implanted intramyocardial tantalum markers. In 35 patients, isovolumic relaxation time was calculated from M-mode tracings selected from two-dimensional echocardiographic recordings. A total of 84 biopsy findings of no rejection, moderate rejection, and severe acute rejection after treatment were correlated with measurements of isovolumic relaxation time. In six patients, end-diastolic volume, end-systolic volume, stroke volume, ejection fraction, and peak filling rate were obtained from biplanar cineradiographic images of intramyocardial markers. Data from 11 prerejection periods were compared with those of moderate acute rejection. All echocardiograms and marker images were analyzed without previous knowledge of biopsy findings. At times of acute rejection, isovolumic relaxation time decreased from 107 to 65 msec (p less than 0.01) and returned to 98 msec after immunosuppressive therapy. Ejection fraction and end-systolic volume did not change significantly with acute rejection, whereas stroke volume decreased from 76 to 67 ml (p less than 0.05). In contrast to the effects on systolic function, episodes of acute rejection were accompanied by a decrease in end-diastolic volume from 166 to 153 ml (p less than 0.01) and a reduction in peak filling rate from 514 to 460 ml/sec (p less than 0.05). These data suggest that acute cardiac rejection is associated with relative preservation of left ventricular systolic performance but with alterations in diastolic dynamics similar to those seen in "restrictive" cardiomyopathy.

Acute Disease↗
PubMed1990

[Acute anterior wall infarct with intractable ventricular fibrillation: successful therapy by recanalization of a left anterior descending coronary artery occlusion].

A 35-year-old male patient was admitted to the intensive care unit of a community hospital with an acute anterior myocardial infarction complicated by initial recurrent episodes of ventricular fibrillation and successful resuscitation. Persistent malignant ventricular arrhythmias during the following days necessitated external defibrillation approximately 250 times. The patient was transferred to the Hannover Medical School, where the occluded left anterior descending coronary artery was successfully recanalized. Eight days later, the malignant ventricular tachyarrhythmias ceased and after 59 days of hospitalization the patient could be discharged in stable condition.

Adult↗
PubMed1989

Intracoronary nisoldipine: effects on acute myocardial ischemia during coronary angioplasty.

The effects on ischemic myocardium of 0.05 mg nisoldipine given by intracoronary injection were studied in 22 patients subjected to percutaneous transluminal coronary angioplasty. The angioplasty balloon was inflated for periods of 60 seconds. During the occlusion period, pulmonary wedge pressure was measured, an intracoronary epicardial ECG recorded, and ventricular volumes and ejection fraction were determined by means of digital subtraction angiography. After the intracoronary administration of nisoldipine, the onset of the rise in diastolic filling pressure was slightly delayed from 29 to 36 seconds. While affecting neither the rise in filling pressure nor the increase in end-diastolic and end-systolic volumes after 60 seconds of ischemia, nisoldipine delayed the occurrence (from 13 to 33 seconds; p less than 0.005) and reduced the extent (from 1.5 to 0.6 mV; p less than 0.001) of ischemic ST elevation in the intracoronary ECG. After nisoldipine, anginal symptoms were clearly reduced during the ischemic phase in the majority of patients. These findings suggest that intracoronary pretreatment with nisoldipine leads to a regional protection of ischemic myocardium without any appreciable effect on ischemia-induced myocardial dysfunction.

Angioplasty, Balloon, Coronary↗
PubMed1988

Effects of intravenous verapamil on left ventricular systolic function and diastolic filling dynamics in patients with coronary artery disease: analysis of intramyocardial markers.

Left ventricular (LV) intramyocardial markers (MM) were used to study the effects of intravenous verapamil on LV pump function and diastolic filling dynamics. Verapamil (0.1 mg/kg bolus followed by 0.005 mg/kg/min) was administered to 10 patients with severe coronary artery disease 4 years after coronary bypass grafting and implantation of 7 tantalum markers into the LV. MM were filmed at 100 frames/sec (biplane 30 degrees RAO/60 degrees LAO). The digitized biplane MM coordinates were transformed into 3-dimensional coordinates and maximal projection area was defined. LV volumes were calculated frame-by-frame and ejection fraction and peak filling rate derived. Pressure-volume relations were calculated in early-, mid-, and end-diastole. Verapamil caused a slight rise in end-diastolic pressure (12 to 14 mmHg, p less than 0.001) and end-diastolic volume (142 to 152 ml; p less than 0.005) and a fall in max dP/dt (1732 to 1570 mmHg/s; p less than 0.01) reflecting the drug's negative inotropic action. Verapamil reduced LV systolic pressure (136 to 126 mmHg; p less than 0.01), diastolic aortic pressure (74 to 68 mmHg; p less than 0.001) and peripheral resistance (1496 to 1348 dynes.s.cm-5; p less than 0.025); cardiac index was increased (2.7 to 2.9 l/min/m2; p less than 0.05), as were ejection fraction (47 to 49%; p less than 0.02) and stroke volume (67 to 75 ml; p less than 0.001). Great cardiac vein flow increased as well (88 to 102 ml/min; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Effects of intracoronary nitroglycerin on coronary vascular volume in man, assessed by a double-indicator dilution technique.

The effects of 0.2 mg nitroglycerin administered directly into the left coronary artery were studied in 7 patients with coronary artery disease. A multipurpose catheter designed for simultaneous measurement of coronary sinus flow and great cardiac vein flow by thermodilution and for addition recording of dye dilution curves by a fiberoptic method was introduced from a right antecubital vein into the coronary sinus and advanced with its tip to the great cardiac vein/anterior cardiac vein juncture. Coronary sinus flow and great cardiac vein flow were measured using the constant infusion technique. Selective bolus injections of indocyanine green dye were measured using the constant infusion technique. Selective bolus injections of indocyanine green dye were performed into the left coronary system via a 8 French Judkins catheter and dye dilution curves were recorded in the upper great cardiac vein. From these curves, coronary transit time was assessed and coronary vascular volume was calculated as great cardiac vein flow times coronary transit time. Intracoronary nitroglycerin led to a transient drop in regional coronary resistance that was associated with an almost parallel increase in intravascular volume. Since this increase in coronary vascular volume exceeded the well-known dilatory effect on the epicardial arteries, and lasted slightly longer than the drop in regional resistance, these data imply that the vasodilatory action of nitroglycerin is different in magnitude as well as in time course in different parts of the coronary circulation.

Blood Volume↗
PubMed1988

[Therapeutic occlusion of an erroneously implanted aortocoronary venous bypass using transluminal balloon embolization].

Today, therapeutic occlusion of blood vessels can be performed not only by surgical ligation, but also by various transluminal embolization techniques. The use of hardly steerable emboli (e.g. metal coils or gel foam) is, however, associated with the risk of embolic displacement into the circulation. The present case describes the embolization of an ACVB-graft erroneously implanted to a cardiac vein, by means of a catheter system with a detachable silicone-rubber balloon (Bard-Parker mini-balloon system).

Angina Pectoris↗
PubMed1987

Late increase in luminal diameter of aortocoronary venous bypass grafts associated with an increase in the vascular region under supply.

In a previous study, a significant inverse relation was found between the luminal size of aortocoronary venous bypass grafts and the vascular resistance of the coronary region that was perfused by the bypass graft in late stages after bypass surgery. This observation suggested that changes in the graft-dependent vascular area could influence the luminal size of the vein graft, even when they occurred several years after operation. Whereas it is well established today that aortocoronary vein grafts often decrease in luminal diameter after implantation, an increase in the bypass lumen has so far not been reported. Therefore, changes in luminal diameter of 27 vein grafts in 21 patients who underwent at least two postoperative angiographic studies (first study 8 +/- 5 months after surgery, second study 58 +/- 32 months after surgery) were compared with the size of the vascular region supplied by the bypass. The graft diameter was found to be unchanged between the two studies (3.3 +/- 0.6 versus 3.4 +/- 0.7 mm, p = NS) when the dependent vascular area was unchanged. A significant increase in graft diameter from 2.8 +/- 0.8 to 3.9 +/- 0.9 mm (p less than 0.001) was observed in nine patients in whom the area of perfusion had increased between the two studies because of the development of occlusion or obstruction of major coronary branches that were now perfused from the grafted vessel by way of collateral vessels. These data support the contention that the luminal size of aortocoronary vein grafts can adapt to the needs of the dependent myocardial vascular region even late after operation rather than being the result of a nonreversible degenerative process as commonly assumed.

Adult↗
PubMed1986

[Acute effect of the cardioselective beta-1-partial agonist, Corwin, on ventricular function and myocardial oxygen consumption in patients with dilated cardiomyopathy].

The effects on left ventricular function and myocardial metabolism of Corwin (ICI 118,587), a selective beta-1 partial agonist, were evaluated in 12 patients with dilated cardiomyopathy. All patients were in sinus rhythm at the time of cardiac catheterization. Immediately before and 20 minutes after intravenous administration of 0.2 mg/kg Corwin over 2 minutes, high-fidelity left ventricular pressures and thermodilution coronary sinus blood flow were recorded along with ventriculograms in the 30 degrees right anterior oblique projection. In 11 patients, Corwin resulted in no change in heart rate, a fall in left ventricular end-diastolic pressure, a rise in left ventricular systolic pressure and an increase in cardiac index. There was a rise in both peak positive and peak negative dP/dt. End-diastolic and end-systolic volume indices fell, and ejection fraction rose. There was an increase in coronary sinus blood flow and a small rise in myocardial oxygen consumption. In contrast to these results in the group as a whole, in one patient Corwin produced depression of both systolic and diastolic left ventricular function. We conclude that, in many patients with dilated cardiomyopathy, Corwin produces an improvement in systolic and diastolic left ventricular function while at the same time only slightly increasing myocardial oxygen demand. In some patients, however, Corwin may result in a significant worsening of left ventricular performance due to its antagonistic effects.

Adrenergic beta-Agonists↗
PubMed1984

[Hemodynamics in ischemia: diastolic phase].

The diastolic portion of the cardiac cycle can be divided into sequential phases: isovolumic ventricular relaxation; rapid ventricular filling; slow, or passive, ventricular filling; and atrial contraction. Contraction and relaxation are to some extent interrelated; however, relaxation is not simply a passive reversal of events during systole. Rather, relaxation is an energy-consuming process which involves dissociation of calcium from the actin-myosin-complex and reuptake of calcium by the sarcoplasmic reticulum. Left ventricular diastolic function is determined by the interrelationship of several/factors, including some intrinsic to the left ventricular chamber (completeness of left ventricular relaxation, time course of left ventricular contraction, and elastic and viscous properties of the myocardium) and others extrinsic to the left ventricle (pericardial and pleural pressure, right ventricular contraction, and coronary perfusion pressure). Acute ischemia alters diastolic left ventricular function by: slowing isovolumic relaxation, delaying left ventricular filling and altering passive elastic properties of the myocardium. Slowing of isovolumic relaxation is measured as a fall in the maximal rate of left ventricular pressure decline (peak negative dP/dt) and as an increase in the time constant (T) of left ventricular pressure fall. Delayed left ventricular filling is manifested regionally as a reduced rate of septal and posterior wall thinning (by echocardiography) and globally as a reduced rate of chamber filling (by gated radionuclide angiography).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1983

Intracoronary nifedipine in human beings: magnitude and time course of changes in left ventricular contraction/relaxation and coronary sinus blood flow.

Eight patients, all men, having at least 75% stenosis of the proximal, middle or both segments of the left anterior descending coronary artery, underwent intracoronary drug studies at the time of cardiac catheterization after saphenous vein bypass grafting. Nifedipine, 0.1 mg dissolved in saline solution, was infused into a left anterior descending graft that was the primary blood supply to each patient's anterior left ventricular wall and septum. High fidelity left ventricular pressure and its first derivative, dP/dt, and aortic pressure were sampled synchronously with coronary sinus blood flow by the thermodilution technique. The time constant of isovolumic pressure decay (T) was derived. In five patients, percent systolic shortening and mean shortening velocity were determined from myocardial markers implanted into the midwall of the myocardium at the time of cardiac surgery. In response to nifedipine, left ventricular systolic pressure decreased and end-diastolic pressure increased up to 60 seconds. Both positive and negative dP/dt also decreased up to 60 seconds, whereas coronary sinus blood flow increased up to 5 minutes. T was increased at 1 minute but returned to baseline by 3 minutes. Percent systolic shortening and mean shortening velocity were decreased at 1 minute but returned to control level by 3 minutes. Thus, although both left ventricular systolic and diastolic function were depressed by intracoronary administration of nifedipine, coronary sinus blood flow was augmented and remained increased long after changes in left ventricular contraction and relaxation had subsided. These temporal differences are consistent with animal studies showing a differential depressant effect of nifedipine on calcium uptake in smooth muscle and cardiac muscle.

Adult↗
PubMed1983

Effects of nitroglycerin on left ventricular diastolic properties in man.

The effects of nitroglycerin (NTG) on left ventricular (LV) isovolumic relaxation and diastolic function were studied in 12 patients with coronary artery disease: in 6 patients after 0.8 mg sublingual (sI) NTG and in 6 patients after 0.15 mg intracoronary (ic) NTG. From high-fidelity LV pressure peak positive and negative dP/dt, LV systolic (LVSP) and end-diastolic pressure (LVEDP) were measured. The time constant T of isovolumic pressure decay was derived from P = a X exp(-t/T) + c. From simultaneous diastolic pressures and volumes, pressure-volume curves were obtained throughout diastole. In an additional 14 patients, the effects of 0.15 mg ic NTG on coronary sinus blood flow (CSBF) and end-diastolic (ED) and end-systolic septal thickness (ESST) were evaluated. SI NTG produced an increase in heart rate and a decrease in LVSP, LVEDP and negative dP/dt. These effects were associated with a decrease in T and a downward shift of the pressure-volume relation. In contrast, ic NTG caused no change in heart rate, LVSP and LVEDP. The LV pressure-volume relation was not altered although T decreased. Ic NTG produced an early rise in CSBF and a sustained increase in EDST and ESST. Data indicate that sI NTG increases the speed of isovolumic relaxation and improves diastolic function, but these actions are not reflected by negative dP/dt due to its dependence on multiple hemodynamic factors. Ic NTG accelerates isovolumic relaxation, but has no measurable effects on later diastolic function. The increase in positive dP/dt may be explained by an engorgement of the coronary vasculature resulting in stretching of the myocardial fibers.

Blood Pressure↗
PubMed1982

Blood velocity, flow and dimensions of aortocoronary venous bypass grafts in the postoperative state.

Intraoperative measurements have suggested an interrelation between the diameter of aortocoronary venous bypass (ACVB) grafts and the hemodynamic properties that may influence the functional results and long-term graft patency. We therefore studied the function of 35 nonobstructed ACVB grafts in 34 patients 1-59 months after bypass grafting. The mean blood velocity and flow were assessed using the roentgen videodensitometric technique. Graft diameters were obtained by morphometry from 35- or 70-mm cineangiograms taken in two orthogonal projections. The regional resistance of the graft-dependent area was calculated as mean aortic pressure/ACVB flow. The average graft diameter was 3.67 mm, the average graft-to-host vessel diameter ratio 1.5, the average ACVB blood velocity 8.5 cm/sec, the average flow 55 ml/min, and the average regional resistance 2.8 mm Hg/ml/min. No significant differences were observed for different graft locations or for different postoperative time intervals. Neither ACVB blood velocity nor flow correlated convincingly with graft size, but there was a significant inverse relation between graft diameter and the resistance of the graft-dependent area. We conclude that ACVB hemodynamics generally cannot be predicted by the dimensions of the graft in the postoperative state. Our data suggest that venous bypass grafts may adjust in size to the needs of the myocardial region supplied by the graft after operation.

Adult↗