Biomedical subjects

X H Krauss

Publications and source records attributed to X H Krauss.

At least 19 recordsLinked to original sources

PubMed2005

Intracardiac pseudotumor caused by mitral annular calcification.

The current report describes a rare case of a pseudotumor in the left ventricle. Transthoracic and transesophageal echocardiography demonstrated a round, echodense, mobile mass attached to the posterior mitral leaflet and annulus. At surgical exploration caseous annular calcification of the posterior mitral leaflet was diagnosed. After resection of the mass, successful mitral valvular plasty was performed. Review of the literature indicated that mitral annular calcification is associated with an increased risk of stroke. Optimal treatment may be surgery, especially when valve plasty can be performed, although randomized trials are currently lacking.

Calcinosis↗

PubMed1999

A structural modeling analysis of anxiety and depression in patients undergoing coronary artery bypass graft surgery: a model generating approach.

The present study is a longitudinal study designed to explore structural relationships between anxiety, depression, personality, and background factors (e.g., gender, age, and complicated medical characteristics) in patients undergoing coronary artery bypass graft (CABG) surgery. At two timepoints before and two after CABG, 217 patients completed self-report questionnaires. To explore structural relationships, the structural equation modeling (SEM) method was applied. Using the model-generating approach, a model was developed, providing a good fit. The structural relationships revealed, in particular, the key position of neuroticism, which was related to both pre- and postoperative anxiety and depression. Relationships between anxiety and depression over time, both intra- and interrelationships, were relatively weak. Relationships between anxiety and depression at the same points in time were relatively strong, with preoperative depression leading to preoperative anxiety, and postoperative anxiety leading to postoperative depression. To provide a useful framework for development of intervention strategies, further research is needed to evaluate the plausibility of the final structural model.

Adult↗

PubMed1998

Delayed increase in high density lipoprotein-phospholipids after ingestion of a fat load in normolipidemic patients with coronary artery disease.

We studied the effect of a single oral fat load, supplemented with retinyl palmitate (RP), on high density lipoprotein (HDL) lipids in six normolipidemic men with coronary artery disease (CAD) and in six age- and lipid-matched controls. All subjects were selected from a study group which underwent the same protocol 2 years earlier. Post-prandial total plasma lipids, plasma RP levels, and HDL lipids were evaluated at 2-h intervals up till 10 h after the meal. In most subjects the post-prandial response of plasma triglyceride (TG) and plasma RP was identical in the first and second tests. Following the fat load, control subjects showed no change in HDL total cholesterol (TC) or HDL cholesteryl ester (CE) and showed an increase in HDL-TG. CAD subjects however showed a decrease in HDL-TC and HDL-CE and an increase in HDL-TG, similar to the increase in control subjects. In control subjects an increase in HDL phospholipid (PL) was apparent between 0 and 8 h after the fat load. By contrast, in CAD subjects the increase in HDL-PL was only found after as long as 6 h. The magnitude of the post-prandial response of HDL-PL measured during the test was significantly lower in the CAD group. The effects of the fat load on HDL free cholesterol (FC) were similar to the changes in HDL-PL. These data support the hypothesis that PL and FC released during the degradation of chylomicrons as surface remnants are taken up by HDL. This process is clearly delayed in normolipidemic CAD subjects compared with controls. The data suggest that differences in the post-prandial response to an oral fat load in normolipidemic CAD patients and control subjects are not confined to the clearance of TG-rich lipoproteins, but also involve a difference in the uptake of chylomicron surface material by HDL.

Adult↗

PubMed1998

The course of anxiety and depression in patients undergoing coronary artery bypass graft surgery.

A semilongitudinal study was designed to follow-up the course of anxiety and depression in patients undergoing coronary artery bypass graft (CABG) surgery. The focus was on possible effects of gender and age on variations in both mean level and interindividual differences over time. At two timepoints before and two after surgery, 217 patients completed self-report questionnaires. Multivariate testing revealed an overall decrease in mean levels of anxiety and depression in the postoperative period but different trends for men and women. Compared with men, women reported more anxiety and depression, both pre- and postoperatively, but showed a relatively stronger decrease in the early postoperative period. Regarding variations in interindividual differences over time, multivariate testing revealed different trends of depression for men and women. Women appeared to be most homogeneous in the early days after surgery, whereas interindividual differences for men showed a stable trend.

Adult↗

PubMed1996

Acute hemodynamic effects and preload-dependent cardiovascular profile of the partial phosphodiesterase inhibitor nanterinone in patients with mild to moderate heart failure.

Nanterinone (UK-61,260) is a novel positive inotropic and balanced-type vasodilating drug, only partially based on phosphodiesterase III inhibition. Preliminary data from controlled studies suggest satisfactory long-term efficacy and safety. As its acute hemodynamic effects in humans are unknown, an oral dose of 2 mg nanterinone was studied in 14 patients with heart failure (NYHA class II-III) on chronic diuretic and angiotensin-converting enzyme (ACE) inhibitor treatment. Before the study, patients were on a 2 g salt-balanced diet, and they received their last medication 16 hours before each study day. Hemodynamic measurements were carried out before and 0.5, 1, 1.5, 2, 2.5, 3, 4, 8, 12, and 24 hours after administration of the study drug. All patients received placebo and nanterinone on 2 consecutive days. Following nanterinone, systemic vascular resistance decreased immediately from 1699 +/- 82 (mean +/- SEM) at baseline to 1368 +/- 80 at 1 hour. Changes persisted for 12 hours. Concomitantly, there was an immediate and significant fall in pulmonary wedge pressure to 38% of baseline at 1.5 hours, together with a 20% reduction in pulmonary artery pressure. Heart rate remained unchanged and arterial pressures showed only a short, significant decrease. Cardiac index rose significantly from 2.28 +/- 0.15 at baseline to a highest value of 2.65 +/- 0.14 1/min/m2 at 1 hour. Changes persisted for 3 hours. Placebo had no effect on these variables. As, in view of its potential venodilating properties, hemodynamic improvement by nanterinone may depend on pre-existing left ventricular filling pressure, patients were subsequently grouped according to baseline pulmonary wedge pressure of > 12 mmHg (H-PCWP) and < or = 12 mmHg (L-PCWP). Cardiac index improved by 26% in H-PCWP and by 17% in L-PCWP (NS). In contrast, PCWP fell more markedly in H-PWCP than in L-PCWP (40% and 23%, respectively, p < 0.05). Thus, oral nanterinone results in a significant acute hemodynamic improvement and is well tolerated. Although changes in left ventricular filling pressure are more pronounced in patients with elevated pre-existing PCWP, cardiac pump function improves equally in patients with normal or low left ventricular filling pressure at baseline.

Aged↗

PubMed1996

Lipoproteins and apolipoproteins in the young and familial risk of coronary atherosclerosis.

The aim of this study was to assess the predictive value of lipoproteins and apolipoproteins at a young age for the development of coronary artery disease at middle and older ages. Because children of coronary artery disease patients are at high risk themselves we compared lipoprotein and apolipoprotein levels between the offspring of parents with and without coronary artery disease. We selected a group of male patients (n = 90), who had severe coronary atherosclerosis at angiography, and a reference group of male controls (n = 62), who had no coronary atherosclerosis at angiography. Lipoprotein and apolipoprotein levels were determined in 115 sons and 73 daughters of the patients with severe coronary atherosclerosis. These were compared to levels in 68 sons and 47 daughters of controls. Additionally, lipoprotein and apolipoprotein levels were compared between patients and controls as well as between their spouses. In sons of patients, lower levels of HDL3 cholesterol (-0.07 mmol/1, standard error of the mean (SEM) 0.03, P < 0.05) and apolipoprotein A2 (-5.1 mg/dl (SEM, 1.4), P < 0.0001) were found compared to sons of controls. Similar differences were observed in daughters of such patients without, however, achieving statistical significance. No significant differences between the groups of offspring were found for total cholesterol, LDL cholesterol, HDL and HDL2 cholesterol, triglycerides and apolipoproteins A-I and B. Patients had higher levels of total (group difference 0.6 mmol/1 (SEM, 0.18), P < 0.001) and LDL cholesterol (0.6 mmol/1 (SEM, 0.17), P < 0.001), triglycerides (0.6 mmol/1 (SEM, 0.16), P < 0.001) and apolipoprotein B (21.2 mg/dl (SEM, 5.1), P < 0.001), and lower HDL cholesterol (0.1 mmol/1 (SEM, 0.04), P < 0.05) than controls. Spouses of patients had higher levels of triglycerides (0.23 mmol/1 (SEM, 0.11), P < 0.05). Our findings add to the growing evidence that predictors for atherosclerotic disease can be detected relatively early in life. It is concluded that reduced levels of HDL3 cholesterol and apolipoprotein A2 may be early risk indicators for coronary atherosclerosis later in life.

Adult↗

PubMed1994

Postprandial triglyceride response in young adult men and familial risk for coronary atherosclerosis.

OBJECTIVE: To determine whether an increased familial risk for coronary artery disease in young adult men is related to changes in postprandial lipoprotein metabolism. DESIGN: Cross-sectional study. SETTING: Coronary angiography departments of four central general hospitals in the Netherlands. PATIENTS: 80 sons (mean age, 24.8 years) of men with severe coronary artery disease and 55 sons (mean age, 23.2 years) of controls. MEASUREMENTS: Postprandial levels of serum triglycerides, retinyl palmitate, and total cholesterol were measured during a 12-hour period after a standardized oral lipid load. RESULTS: Both groups showed a marked increase in levels of serum triglyceride and retinyl palmitate after lipid loading, reaching a maximum 4 to 6 hours postprandially. No changes in postprandial total cholesterol levels were observed in either group. Sons of men with coronary artery disease had prolonged postprandial hypertriglyceridemia when compared with sons of controls. Significant differences in postprandial triglyceride levels were found at 8 hours (difference, 0.35 mmol/L; 95% CI, 0.07 to 0.62 mmol/L), at 10 hours (difference, 0.21 mmol/L; CI, 0.06 to 0.36 mmol/L), and at 12 hours after lipid loading (difference, 0.13 mmol/L; CI, 0.01 to 0.26 mmol/L). Levels of postprandial retinyl palmitate were also slightly, but not statistically, different (mainly after 6 hours). CONCLUSIONS: Healthy young adult sons, whose fathers have established coronary artery disease, have prolonged postprandial hypertriglyceridemia. Changes in postprandial lipoprotein metabolism appear to be associated with familial risk for coronary atherosclerosis.

Adult↗

PubMed1994

Acute systemic and antiischemic effects of epanolol in patients with coronary artery disease.

Antiischemic effects of beta 1-blocking agents are based on intrinsic negative inotropic and chronotropic properties. Partial beta 1-agonistic activity, although useful in preserving cardiac function, may counteract such antiischemic properties by modulating the intrinsic negative cardiac effects of beta-blockade. To investigate the acute hemodynamic and antiischemic profile of epanolol, a cardioselective beta 1-antagonist and partial agonist, 20 patients with left coronary artery disease underwent two incremental atrial pacing tests, 45 minutes before (APST I) and 15 minutes after (APST II) 4 mg intravenous epanolol, administered over 5 minutes. Additional measurements were carried out at 1, 3, 5, 10, and 15 minutes after epanolol, at basal and fixed heart rates. Epanolol immediately reduced heart rate with a maximum of 10% at 15 minutes and decreased contractility (Vmax) by 7% (both p < .05), whereas cardiac output fell temporarily by 9% (p < .05). Other hemodynamic parameters did not change, except for a significant 11% reduction in myocardial oxygen demand. Despite comparable pacing conditions, both the double product and contractility decreased significantly less during APST II, resulting in a 17% lower myocardial oxygen consumption (p < .05). Myocardial ischemia was markedly reduced, indicated by normalization of lactate metabolism [lactate extraction 16 +/- 7% vs. -7 +/- 8% (APST I)], less ST depression (21%), and modulation of LV end-diastolic pressure postpacing (all p < .05 vs. APST I), whereas angina was absent or less in 14 patients. None of the patients reported an adverse effect. Thus, under resting conditions intravenous epanolol induces moderate, short-lasting negative chronotropic and inotropic effects, but does not alter cardiac pump function or vascular resistance, reflecting its additional beta 1-agonistic properties. Alternatively, during pacing it still reduces ischemia through negative inotropic effects and diminishes myocardial oxygen demand, reflecting its beta 1-antagonistic profile.

Adrenergic beta-1 Receptor Agonists↗

PubMed1994

Hemodynamic, neurohumoral, and myocardial energetic effects of pimobendan, a novel calcium-sensitizing compound, in patients with mild to moderate heart failure.

In contrast to cyclic AMP-dependent positive inotropes, the calcium-sensitizer and partial phosphodiesterase (PDE) inhibitor pimobendan may induce beneficial effects in heart failure. However, its effect on relaxation, myocardial energetics and neurohormones are unknown. Twelve patients with heart failure, New York Heart Association (NYHA) classification II-III, due to ischemic cardiomyopathy, were studied for 1 h after they received 5 mg pimobendan intravenously (i.v.). Pimobendan progressively reduced systemic resistance and left ventricular end-diastolic pressure (LVEDP) (22 and 50%, respectively) and improved isovolumetric contractility and relaxation parameters by 30% (all p < 0.05 vs. control). LV end-diastolic and end-systolic volumes (LVEDV, LVESV) decreased significantly by 20 and 19%, respectively. Cardiac output (CO) increased by 17% due to a simultaneous increase in heart rate (HR) from 75 +/- 3 to 86 +/- 5 beats/min (mean +/- SEM, p < 0.05). Pimobendan did not change coronary hemodynamics, but myocardial O2 extraction and consumption were decreased significantly by 18 and 20%, respectively. Catecholamines, angiotensin II (AII), and aldosterone levels did not change significantly. In contrast, arterial and coronary venous renin increased significantly from 57 +/- 17 and 53 +/- 14.7 microM/h at control to 69 +/- 20 and 69 +/- 20 microM/h, respectively, 60 min after pimobendan administration. Simultaneously, cardiac renin uptake at baseline (0.449 +/- 0.185 mumol/min) changed to release (-0.071 +/- 0.145 mumol/min, p < 0.05). Serious side effects did not occur. Thus, pimobendan had progressive positive inotropic and lusitropic effects, diminished preload and afterload despite modest stimulation of plasma renin activity (PRA), and reduced systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Hemodynamic tolerability and anti-ischemic efficacy of high dose intravenous diltiazem in patients with normal versus impaired ventricular function.

OBJECTIVES: This study was designed to compare the acute systemic and coronary hemodynamic effects of high doses of intravenous diltiazem in patients with normal versus impaired left ventricular function, investigate the safety of this drug and compare its anti-ischemic potential in these two patient groups during pacing-induced stress. BACKGROUND: Because coronary hemodynamic effects and negative inotropic properties of diltiazem are dose related, high dose intravenous diltiazem may improve anti-ischemic efficacy but may not be tolerated in patients with impaired cardiac function. METHODS: High dose intravenous diltiazem, 0.4 mg/kg for 5 min followed by 0.4 mg/kg for 10 min, was administered to 23 normotensive patients with coronary artery disease, 11 (group A) with normal and 12 (group B) with impaired ventricular function (ejection fraction < 45%) during two identical arterial pacing stress tests performed 30 min before (pacing test I) and immediately after diltiazem (pacing test II). RESULTS: Diltiazem was well tolerated despite high peak plasma levels, 869 +/- 152 micrograms/liter (group A) and 926 +/- 169 micrograms/liter (group B). It resulted in immediate but similar reductions in systemic resistance from 1,321 +/- 136 (control value) to 963 +/- 113 dynes.s.cm-5 (group A) and from 1,267 +/- 106 to 865 +/- 58 dynes.s.cm-5 (group B) and in mean arterial pressure from 107 +/- 3 to 93 +/- 4 mm Hg (group A) and from 103 +/- 4 to 86 +/- 4 mm Hg (group B), at 5 min after diltiazem (all p < 0.05 vs. control value). Diltiazem improved stroke output from 36 +/- 3 (control value) to 46 +/- 4 ml/beat per m2 in group B and from 44 +/- 4 (control value) to 49 +/- 5 ml/beat per m2 in group A, an effect that was significantly greater and more prolonged in group B than in group A. Although neither heart rate nor contractility was affected in either group, left ventricular end-diastolic pressure increased in group A (9 +/- 2 mm Hg to 12 +/- 1 mm Hg, p < 0.05) but not in group B. Despite similar reductions in coronary resistance and improvements in coronary flow, diltiazem consistently reduced myocardial oxygen extraction, but only in group B. Also, the anti-ischemic effects of diltiazem were more pronounced in group B. During pacing test II, myocardial lactate extraction normalized in group B (7 +/- 5% vs. -6 +/- 12% [pacing test I]) but not in group A, contractility indexes improved more and the increase in left ventricular filling pressure was reduced to a greater extent in group B. Moreover, the ischemia-induced increase in arterial pressures, observed in both groups during pacing test I, was prevented in group B but recurred in group A during pacing test II. CONCLUSIONS: High dose intravenous diltiazem is well tolerated, augments coronary flow and improves left ventricular pump function, particularly in patients with preexisting ventricular dysfunction. As its anti-ischemic effects also appear more pronounced in the latter group, high dose diltiazem may be particularly useful when ventricular function is depressed, for example, during prolonged ischemia at rest.

Cardiac Catheterization↗

PubMed1991

Magnetic resonance imaging of myocardial infarction: correlation with enzymatic, angiographic, and radionuclide findings.

Spin-echo cardiac magnetic resonance imaging studies were performed in 20 patients with a first 7- to 14-day-old (mean 10) myocardial infarction. The magnetic resonance imaging findings were compared with coronary angiography (14 patients), myocardial enzyme release (18 patients), radionuclide angiography (19 patients), and thallium-201 perfusion scintigraphy (19 patients). Regional T2 relaxation times determined from the signal intensities at echo times 30 msec and 90 msec were significantly prolonged in the infarcted areas. Based on abnormal T2 times for every patient, a regional and a total myocardial damage score was determined. The infarct-related artery was correctly identified in 93% of patients by magnetic resonance imaging, in 79% of patients by thallium-201 scintigraphy, and in 62% of patients by radionuclide angiography. The total damage score correlated well with enzymatic infarct size (r = 0.75, p less than 0.001). The correlation between left ventricular end-systolic volume index determined by magnetic resonance imaging and by radionuclide angiography was r = 0.89 (p less than 0.002). The left ventricular end-systolic volume index correlated significantly with enzymatic infarct size (r = 0.72, p less than 0.001), total damage score (r = 0.68, p less than 0.002), and radionuclide left ventricular ejection fraction (r = -0.68, p less than 0.002). Correlations between the magnetic resonance damage score and the thallium-201 perfusion score were r = 0.60 (p less than 0.01) for the exercise images, and r = 0.72 (p less than 0.001) for the redistribution images. This study shows that spin-echo magnetic resonance imaging is quite comparable with the established noninvasive imaging modalities currently used in patients with acute myocardial infarction.

Adult↗

PubMed1991

Hemodynamic effects and tolerability of intravenous amiodarone in patients with impaired left ventricular function.

Acute hemodynamic effects and tolerability of intravenous amiodarone, 5 mg/kg administered over 5 minutes, were compared in patients with coronary artery disease and either a normal (left ventricular [LV] ejection fraction greater than or equal to 45%, n = 10, group N) or impaired LV function (ejection fraction less than 45%, n = 9, group L). Amiodarone reduced systemic vascular resistence and LV and aortic pressures in both groups (13%, 18%, and 13%, respectively [group N], and 15%, 17%, and 15%, respectively [group L]) over the short term. Heart rate initially increased (18%, group L, and 10% group N), but was followed by a late 6% decrease in group N only, and by a progressive reduction in contractility (Vmax), together with a rise in LV end-diastolic pressure (19% and 38%, respectively [group N] and 17% and 58%, respectively [group L]; all values p less than 0.05 versus control). Coronary flow increased significantly by 20% (group N) and 31% (group L), but only during amiodarone administration, accompanied by a 26% and 25% reduction in myocardial oxygen extraction in groups N and L, respectively. Stroke work decreased in both groups (20% [group N] and 19% [group L], p less than 0.05 versus control). In contrast, cardiac output only improved (10%) in patients with impaired ventricular function. Significant side effects did not occur. Thus relatively high dosages of intravenous amiodarone are well tolerated and improve cardiac pump function in patients with an impaired, but not with a normal cardiac function. However, the tendency to increase LV end-diastolic pressures necessitates careful monitoring in patients in whom preexisting LV filling pressure may be elevated.

Adult↗

PubMed1990

[Early thrombolysis improves the long-term prognosis for patients with a heart infarct].

In a previously reported clinical study treatment of myocardial infarction with intracoronary streptokinase (269 patients) was compared with conventional therapy (264 patients). To determine the long-term effects of thrombolytic therapy patient data were collected from 3 to 7 years after admission. Three-year survival rates were 87% after thrombolysis and 79% after conventional therapy. Bypass surgery was done in 19% versus 16%, and PTCA in 9% versus 6% of patients. Patients treated with thrombolysis also had a better prognosis after discharge. The difference in survival between the two treatment groups was 6% after 1 year and 10% after 5 years. Benefit was largest in patients with an anterior infarction, patients with extensive myocardial ischaemia and patients treated shortly after onset of infarction. Left ventricular function appeared to be the best determinant predicting survival after discharge. The findings show that early thrombolysis after acute myocardial infarction also results in improved long-term survival.

Aged↗

PubMed1990

Duration and reproducibility of initial hemodynamic effects of flosequinan in patients with congestive heart failure.

The duration and reproducibility of hemodynamic effects of flosequian, a direct-acting, balanced-type vasodilator, were studied in 19 heart failure patients (NYHA class 3.0 +/- 0.7) receiving 100 mg orally (day 1), placebo (day 2), and again 100 mg (day 3). Flosequinan immediately reduced systemic and pulmonary resistance (23% and 35%, respectively, at 60-90 minutes postdrug) and decreased pulmonary wedge, right atrial, mean pulmonary artery, and mean arterial pressure by 38%, 50%, 25%, and 7%, respectively. Concomitantly, cardiac output, and stroke volume and work increased by 26%, 20%, and 22%, respectively. Most hemodynamic effects persisted for 48 hours. In contrast, changes in pulmonary wedge and arterial pressures, stroke volume, and stroke work only lasted for 2-12 hours. Maximum absolute changes on day 3 were generally comparable with first-dose effects with, again, long-lasting effects on systemic resistance and cardiac output. However, changes in pulmonary artery, wedge, and resistance were significantly shorter than after first dose administration. These data indicate sustained and reproducible arterial dilating effects of flosequinan, but less pronounced and shorter lasting pulmonary arterial and venodilator properties.

Aged↗

PubMed1990

Neurohumoral activation during acute myocardial ischaemia. Effects of ACE inhibition.

ACE inhibition may be useful in several manifestations of ischaemic heart disease, such as heart failure due to ischaemic cardiomyopathy. Recent evidence suggests that these effects may also be present in normotensive patients with ischaemic heart disease without heart failure. Theoretically, converting-enzyme inhibition, through coronary and systemic vasodilating effects and negative inotropic properties, should have a favourable effect on the myocardial oxygen supply/demand ratio and, hence, affect the incidence and severity of myocardial ischaemia. It is doubtful, however, whether these cardiac and extracardiac properties of ACE inhibitors really underlie its potential antiischaemic effects, at least in the average patient with ischaemic heart disease without concomitant heart failure and hypertension. Recent animal and human studies indicate that converting-enzyme inhibitors may modulate myocardial ischaemia by reducing ischaemia-induced circulating neurohumoral activation. It has been shown that, depending on the severity of ischaemia, the circulating renin-angiotensin system may become activated together with an increase in circulating catecholamine levels. ACE inhibition suppresses this neuroendocrine stimulation during ischaemia and modulates subsequent systemic and, presumably, also coronary vasoconstriction. In addition to these effects on circulating neurohormones, ACE inhibition could affect myocardial ischaemia through a number of local actions, e.g. modulation of tissue (cardiac) angiotensin II formation and bradykinin breakdown, stimulation of prostaglandin synthesis and, in the use of sulphydryl compounds, by affecting EDRF formation. Whether ACE inhibitors have clear antiischaemic effects in all clinical conditions is uncertain. Their efficacy to limit exercise-induced ischaemia has been questioned. In contrast, pacing-induced ischaemia in patients at rest is clearly prevented by ACE inhibition. This differential effect may be related to a more pronounced difference in circulating neurohormones during exercise per se. It also suggests that ACE inhibitors may be particularly useful as (additional) antiischaemic therapy in patients with angina at rest, e.g. unstable angina and the acute phase of myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1989

Acute hemodynamic and antiischemic properties of intravenous bepridil in coronary artery disease.

The acute hemodynamic and antiischemic effects of intravenous bepridil (3 mg/kg/5 minutes followed by 1 mg/kg/hour) were studied in 19 patients with coronary artery disease under basal conditions and during 2 identical pacing stress tests 30 minutes before (pace test I) and 15 minutes after (pace test II) onset of infusion. Bepridil immediately decreased coronary and systemic vascular resistance (26 and 17%, respectively). This resulted in a 19 and 21% reduction in left ventricular systolic and mean aortic pressures and a 15% increase in coronary flow and stroke index (p less than 0.05 vs control for each). These vasodilating effects were short lasting, persisting for 5 minutes after the bolus infusion, followed by significant reductions in heart rate (15%) and contractility (10%) and a temporary 46% increase in left ventricular filling pressure. During both pace tests heart rate, contractility, coronary flow and myocardial O2 consumption were comparable. In contrast, bepridil prevented the significant increase in systemic resistance and mean aortic pressure observed during pace test I (11 and 15%, respectively). Subsequently, myocardial O2 demand was significantly less during pacing after bepridil, due to an 11% reduction in left ventricular systolic pressure (p less than 0.05 vs control and pacing test II vs I). This resulted in marked antiischemic effects: normalization of lactate extraction and reduction in ST-segment depression (-14 +/- 7 vs 3 +/- 6% and 0.2 +/- 0.02 vs 0.13 +/- 0.02 mV, respectively, pace test I vs II, p less than 0.05), and in less or no angina in 18 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Long-term benefit of early thrombolytic therapy in patients with acute myocardial infarction: 5 year follow-up of a trial conducted by the Interuniversity Cardiology Institute of The Netherlands.

Patients (n = 533) who participated in the Interuniversity Cardiology Institute of the Netherlands Trial were followed up for 3 to 7 years. The 5 year survival rate after thrombolytic therapy with intracoronary streptokinase was 81% (269 patients) compared with 71% after conventional therapy (264 patients). The greatest improvement in survival was observed in patients with anterior infarction (81% versus 64% with thrombolytic therapy or conventional therapy, respectively), in those with heart failure on admission or a previous infarction and in those with extensive myocardial ischemia on admission. Left ventricular ejection fraction at the time of hospital discharge was better after thrombolytic therapy. In the hospital survivors, long-term outcome was related to left ventricular function at the time of discharge and, to a lesser extent, to the underlying coronary artery disease. The initial therapy (thrombolysis or conventional) was not an independent additional determinant of long-term survival when left ventricular function and coronary status at the time of hospital discharge were taken into account. Thus, the salutary effects of thrombolytic therapy appear to be the result of myocardial salvage. Reinfarction within 3 years was observed more frequently after thrombolytic therapy, particularly in patients with inferior wall infarction and those with greater than or equal to 90% stenosis of the infarct-related vessel at discharge. Coronary bypass surgery and coronary angioplasty were performed more frequently after thrombolytic therapy than in conventionally treated patients. At 5 years, approximately 40% of patients in both groups had an uneventful course without reinfarction or additional revascularization procedures. These observations demonstrate that the benefits of thrombolytic therapy are maintained throughout 5 years of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗

PubMed1988

Relation between infarct size and left ventricular performance assessed in patients with first acute myocardial infarction randomized to intracoronary thrombolytic therapy or to conventional treatment.

Reperfusion of ischemic myocardium has been reported to increase the cumulative creatine kinase activity in plasma per gram of infarcted myocardium as assessed with the method of Shell et al. In an attempt to find out whether infarct size assessment using the method of Witteveen et al was affected by reperfusion, the relation between enzymatic infarct size was analyzed using Witteveen's method and left ventricular (LV) function parameters in 266 patients with first acute myocardial infarction randomized to intracoronary thrombolysis (n = 134) or conventional therapy (n = 132). Compared with patients allocated to conventional therapy, patients allocated to intracoronary thrombolysis had smaller enzymatic infarct size by 29% (p less than 0.001), smaller LV end-diastolic and end-systolic volume indexes by 10% (p less than 0.05) and 20% (p less than 0.005), respectively, and higher LV ejection fraction (55 +/- 1% vs 49 +/- 1%; p less than 0.001). The beneficial effects of thrombolytic therapy on LV performance were closely associated with thrombolysis-induced limitation of infarct size. The dependence from infarct size of LV end-diastolic volume, LV end-systolic volume, and ejection fraction was not different in the 2 therapy groups. It was concluded that Witteveen's method of infarct size assessment is not influenced by the presence of reperfusion. Therefore, this method was recommended for trials on recanalization in patients with acute myocardial infarction.

Angiography↗