PubMed HealthSearch

Biomedical subjects

I Amende

Publications and source records attributed to I Amende.

At least 19 recordsLinked to original sources

Intracellular calcium and ventricular function. Effects of nisoldipine on global ischemia in the isovolumic, coronary-perfused heart.

Ischemia-induced ventricular dysfunction has been shown to be associated with increased diastolic and systolic intracellular concentrations of free, ionized calcium ([Ca2+]i). The present study was designed to determine the effects of the Ca2+ antagonist nisoldipine on the relationship between [Ca2+]i and left ventricular contraction and relaxation during ischemia and reperfusion on a beat-to-beat basis. Nine isovolumic coronary-perfused ferret hearts were made globally ischemic for 3 min and reperfused for 10 min. Ischemia and reperfusion were repeated during perfusion with a buffer containing 10(-8) M nisoldipine. From left ventricular developed pressure, time to peak pressure and time to 50% pressure decline were obtained. [Ca2+]i was determined with the bioluminescent protein aequorin. Global ischemia caused a rapid decline in contractile function and a significant increase in diastolic [Ca2+]i, from 0.35 to 0.81 microM, and in systolic [Ca2+]i, from 0.61 to 0.96 microM. During reperfusion, [Ca2+]i returned to baseline while ventricular function was still impaired. Relaxation was more affected than systolic contractile function. Nisoldipine significantly reduced the ischemia-induced rise in diastolic [Ca2+]i to 0.62 microM, and in systolic [Ca2+]i to 0.77 microM, and lessened the decrease in contractile function. Nisoldipine significantly accelerated the decline in [Ca2+]i during reperfusion and improved recovery of contractility and relaxation. These effects were associated with a significant diminution in ischemic lactate production. Taken together, our results provide direct quantitative evidence on a beat-to-beat basis that the calcium antagonist nisoldipine can ameliorate ischemia-induced abnormalities in [Ca2+]i handling, an effect that was associated with improved myocardial function during early reperfusion.

Animals

Ventricular function and calcium handling during ischemia.

Ischemia-induced ventricular dysfunction has been shown to be associated with increased diastolic and systolic intracellular concentrations of free, ionized calcium ([CA2+]i). The present study was designed to determine the effects of the calcium antagonist nisoldipine on the relationship between [Ca2+]i and left ventricular contraction and relaxation during ischemia and reperfusion on a beat-to-beat basis. Nine isovolumic coronary-perfused ferret hearts were made globally ischemic for 3 min and reperfused for 10 min. Ischemia and reperfusion were repeated during perfusion with buffer containing 10(-8) M nisoldipine. From the left ventricular developed pressure, the time to peak pressure and time to 50% pressure decline were obtained. [Ca2+]i was determined with the bioluminescent protein aequorin. Global ischemia caused a rapid decline in contractile function and a significant increase in diastolic [Ca2+]i from 0.35 to 0.81 microM and in systolic [Ca2+]i, from 0.61 to 0.96 microM. During reperfusion, [Ca2+]i returned to baseline while ventricular function was still impaired. Relaxation was more affected than systolic contractile function (Fig. 1). Nisoldipine significantly reduced the ischemia-induced rise in diastolic [Ca2+]i to 0.62 microM and in systolic [Ca2+]i to 0.77 microM and lessened the decrease in contractile function. Nisoldipine significantly accelerated the decline in [Ca2+]i during reperfusion and improved recovery of contractility and relaxation. These effects were associated with a significant diminution in ischemic lactate production. Taken together, our results provide direct quantitative evidence on a beat-to-beat basis that the calcium antagonist nisoldipine can ameliorate ischemia-induced abnormalities in [Ca2+]i handling, an effect that was associated with improved myocardial function during early reperfusion.

Animals

Percutaneous transluminal angioplasty of aortocoronary venous bypass grafts and effect of the caliber of the grafted coronary artery on graft stenosis.

The influence of morphologic parameters on the recurrence of stenosis after percutaneous transluminal coronary angioplasty of 49 stenoses in aortocoronary venous bypass grafts of 41 patients was investigated. Vessel dimensions were measured quantitatively. Angioplasty was successful in 46 stenoses (94%) of 38 patients (93%). In 35 patients (92% of successfully treated patients) with 42 stenoses, control angiography was performed after a mean interval of 189 +/- 186 days. In 9 patients (26%), 9 stenoses (21%) had recurred. The diameter of the grafted coronary artery distal to the anastomosis was significantly smaller in grafted arteries with than without recurrent stenoses (1.92 +/- 0.52 vs 2.45 +/- 0.50 mm; p less than 0.01). Recurrence also correlated with the ratio between graft diameter and coronary artery diameter greater than 1.35 (p less than 0.02) and with the stenosis length greater than 10 mm before angioplasty (p less than 0.01). Graft age, graft diameter and stenosis location in the graft had no significant influence on recurrence. Thus, the diameter of the grafted coronary artery and the length of the critical stenosis are parameters for recurrence after angioplasty of graft stenoses and should be considered in the selection of patients for this intervention.

Aged

The effects of pretreatment with nitroglycerin on ischemic left ventricular dysfunction during coronary angioplasty.

To evaluate the degree to which nitroglycerin reduces myocardial ischemia and dysfunction induced by transient coronary occlusion, 19 patients were studied during coronary angioplasty of the left anterior descending coronary artery. After a control occlusion of 60 seconds, 0.2 mg nitroglycerin was administered intravenously and the occlusion was repeated for 60 seconds. Before and during the occlusion period, pulmonary capillary wedge pressure was measured, the intracoronary ECG was recorded, and ventricular volumes, ejection fraction, and regional systolic shortening were obtained by digital subtraction angiography. Nitroglycerin caused a significant fall in pulmonary capillary wedge pressure before (10 vs. 7 mmHg) and at 60 seconds occlusion (18 vs. 14 mmHg), but did not significantly delay the rise in wedge pressure (37 vs. 44 seconds). End-systolic left ventricular volume at 60 seconds of occlusion was reduced by nitroglycerin (77 vs. 68 ml), whereas regional shortening of the ischemic segments remained unchanged (22 vs. 23%). Nitroglycerin did not delay the onset of ischemic ST-segment elevation (14 vs. 14 seconds) and had no effect on the changes of ST elevation in the intracoronary ECG (1.9 vs. 1.9 mV). These findings suggest that intravenous nitroglycerin reduces filling pressure and slightly improves left ventricular global function during acute coronary occlusion. Nitroglycerin, however, has little effect on ischemia-induced regional dysfunction and on ST-segment elevation in the intracoronary ECG.

Adult

Angioplasty of subacute and chronic total coronary occlusions: success, recurrence rate, and clinical follow-up.

Angioplasty of single total, subacute, or chronic coronary occlusions was performed in 90 patients. It was successful in 54 occlusions (60%), in 77% of those less than 6 weeks old, and in 44% of those of greater than 6 weeks' duration (p less than 0.005). All procedures were uneventful. Control angiography was performed in 53 (98%) patients with successful angioplasty after an average interval of 97 +/- 53 days. Stenosis had recurred in 16 patients (30%). During a follow-up period of 36 +/- 13 months, three patients died, five patients underwent coronary bypass operation, and 10 had reangioplasty. Despite an additional late angiographic recurrence of stenosis in seven patients, 36 patients revealed angiographic long-term success. In the 46 nonoperated patients, angina pectoris and exercise stress tests were substantially improved. Thus angioplasty of subacute and chronic total coronary occlusions is an uneventful procedure, the success rate depending on the duration of the occlusions. Despite a high angiographic recurrence rate, the angiographic and clinical long-term results are favorable.

Adult

[Percutaneous, transluminal angioplasty of aortocoronary venous bypass grafts--acute success, angiography and clinical follow-up].

In 41 consecutive patients with 49 stenoses of aorto-coronary venous bypass (ACVB) grafts percutaneous transluminal angioplasty (PTA) was attempted. PTA was successful, i.e., the percent area stenosis was reduced by greater than 20% to less than 70% (quantitative measurement with a precision magnifying lens from two orthogonal angiographic views) in 46 stenoses (94%) of 38 patients (93%). In 35 patients (92%) with 42 stenoses control coronary angiography was performed after a mean interval of 189 +/- 186 days. Recurrence, defined as an increase of percent area stenosis to greater than or equal to 70%, was found in nine stenoses (21%) of nine patients (26%). Recurrence correlated with a stenosis length greater than 10 mm before PTA (5/8 vs 4/32 stenoses: p less than 0.01). In recurrent stenoses, the average diameter of the grafted native coronary artery was significantly smaller than in recurrence-free stenoses (1.92 +/- 0.52 mm vs 2.45 +/- 0.50 mm; p less than 0.01). Clinical data were collected from all 38 patients with successful PTA after an average of 30 +/- 17 months following PTA. In this interval, 11 patients had undergone re-angioplasty and eight patients were re-operated; in addition, there were three cardiac deaths. In the 27 surviving patients without re-operation (71%), angina pectoris had improved from a mean of 3.0 +/- 0.7 before PTA to 1.8 +/- 1.0 (CCS-classification) (p less than 0.001). In 19 of the 27 patients (70%) the exercise stress test was negative, in contrast to only three patients (11%) before PTA. Thus, in the majority of patients PTA of ACVB-graft stenoses improves quality of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Comparison of three different principles in the assessment of coronary flow reserve from digital angiograms.

In 70 patients without coronary disease we have compared three different principles to assess coronary flow reserve during diagnostic heart catheterization. Digital angiograms with ECG-triggered bolus injections of 4 to 8 ml of contrast medium at rest and after stimulation by dipyridamole (0,5 mg/kg i.v.) or papaverine (12,5 mg i.c.) were acquired in a 512 x 512 matrix at 8 bit resolution (ADAC 4100) and stored on a digital disk at 25 frames/sec. or 2 frames/cardiac cycle (PPR-mode). Angiograms were processed by cyclic R-wave-gated mask mode subtraction and coronary flow in the LAD area was assessed by three different approaches: 1. A traditional densitometric principle. 2. The 'CMAP' principle. 3. A modification of the Stewart-Hamilton principle comparing the total amount of contrast medium that enters the coronary circulation to the area of the contrast dilution curve in a fixed portion of the LAD. Flow was measured simultaneously during angiography using the thermodilution technique for coronary sinus/great cardiac vein flow. Drug stimulation resulted in an increased coronary blood flow up to five times of resting flow. Regression analysis revealed the following results for the assessment of the coronary flow reserved by digital angiography (y) when compared to thermodilution (x): [table: see text] Method 2 could be improved by replacing the density factor by morphometrically measured proximal LAD volume (y = 0.77x + 0.55; r = 0.78; SEE = +/- 0.43). In conclusion, our data suggest that the Stewart-Hamilton principle may be advantageous over time parameter-dependent approaches in the assessment of coronary flow reserve by digital angiography.

Adult

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

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

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

[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

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

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

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

[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

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

[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