PubMed Health⌕ Search

Biomedical subjects

J Vanhaecke

Publications and source records attributed to J Vanhaecke.

At least 55 records · Page 3Linked to original sources
PubMed1994

Safety and efficacy of low dose simvastatin in cardiac transplant recipients treated with cyclosporine.

Hyperlipidemia is common in heart transplant patients. Lipid-lowering therapy poses special problems, yet may be important because accelerated graft atherosclerosis is the major factor limiting long-term survival. Simvastatin 5 mg/day was started > 6 months after surgery in 26 consecutive cardiac transplant recipients with a total serum cholesterol level of > 250 mg/dl. The dose of simvastatin was increased in 5-mg increments until total serum cholesterol fell below 220 mg/dl or until side effects developed or up to a maximal dose of 20 mg/day. The final average daily dose was 10 mg. Changes in serum lipid levels after 6 months of therapy were compared with data from a matched and concurrent control group of heart transplant patients not taking simvastatin. Immunosuppression for both groups consisted of CsA, AZA, and corticosteroids. In the simvastatin-treated group, the serum level of total cholesterol decreased by 27% from 315 +/- 53 to 230 +/- 38 mg/dl (P < 0.0001), low density lipoprotein cholesterol decreased by 40% from 205 +/- 30 to 123 +/- 32 mg/dl (P < 0.0001), and triglycerides decreased by 21% from 177 +/- 89 to 140 +/- 49 mg/dl (P < 0.01). There was no significant change in high density lipoprotein cholesterol level. Body weight and CsA blood levels remained stable. Steroid intake decreased during the study period to a similar extent in both the treated and the control groups. In the control group, no significant changes in serum lipid levels were observed. Two patients experienced a mild form of myotoxicity. In one other patient simvastatin treatment was stopped after an acute pancreatitis of uncertain etiology developed. Low dose simvastatin effectively lowers total serum cholesterol, low density lipoprotein cholesterol, and triglycerides in heart transplant patients. With due precautions, the safety profile of the drug in this patient population seems reasonable.

Anticholesteremic Agents↗
PubMed1994

Effects of oral pretreatment with metoprolol on left ventricular wall motion, infarct size, hemodynamics, and regional myocardial blood flow in anesthetized dogs during thrombotic coronary artery occlusion and reperfusion.

OBJECTIVES: To study the effects of oral pretreatment with metoprolol over 3 days on hemodynamics, left ventricular function, regional myocardial blood flow, and infarct size in an anesthetized dog model of thrombotic occlusion of the anterior descending coronary artery treated with thrombolysis. METHODS: Ten dogs received 200 mg metoprolol (Selozok) orally and 8 dogs received placebo for 3 days twice daily and 1 hour before the experiment. Under general anesthesia, thrombotic occlusion was provoked by the copper-coil technique. Intracardiac pressures and their derivatives, cardiac output (thermodilution method), regional coronary blood flow (microspheres), global and regional left ventricular function (ventriculography), and infarct size (triphenyltetrazolium staining) were measured. Measurements were performed during control, after 60 minutes of occlusion, and after 30 and 90 minutes of reperfusion. Thrombolysis was performed in all dogs 60 minutes after occlusion by intravenous infusion of 10 micrograms/kg/min of rt-PA for 30 minutes. RESULTS: During control cardiac output was lower, total peripheral resistance higher, and Tau and the left ventricular isovolumic relaxation time greater in the metoprolol group. During occlusion and after reperfusion, there were no significant hemodynamic differences between both groups. Blood flow to the area at risk and circumflex territory during occlusion were, respectively, 12.8 +/- 5.80 ml/100 g/min versus 9.65 +/- 8.35 ml/100 g/min (p > 0.05) and 42.58 +/- 7.86 ml/100 g/min versus 61.52 +/- 20.43 ml/100 g/min (p = 0.01) in the metoprolol- and placebo-treated dogs. The ratios of flow area at risk/circumflex territories in the epicardial, midmyocardial, and endocardial layers were, respectively, 0.44 +/- 0.20, 0.19 +/- 0.09, and 0.20 +/- 0.13 in the metoprolol- versus 0.24 +/- 0.16, 0.08 +/- 0.06, and 0.06 +/- 0.07 (p > or = 0.04) in the placebo-treated dogs. The ratio of flow endocardium/epicardium was higher (p > or = 0.02) in the active treatment group during the control period, both in the area at risk and circumflex territory; this was also the case in the circumflex territory at the end of the experiment (p = 0.003). Thirty minutes after occlusion, blood flow to the three layers of the area at risk rose to 2-3 times control values in both groups; a significant increase above control values also occurred in the circumflex territory. After 90 minutes reperfusion, blood flow to both territories was similar in both groups but was comparable to the control; however, in necrotic tissue of the subendocardial layer of both groups, flow fell below control values (p < 0.05). End-systolic volume rose from 21.2 +/- 7.4 ml to 36.1 +/- 11.5 ml (p < 0.05), end-diastolic volume remained constant (46.0 +/- 13.8 vs. 47.9 +/- 12.1 ml; p > 0.05), and ejection fraction fell from 53.9 +/- 8.3% to 25.8 +/- 10.2% (p < 0.05) at the end of the experiment in the metoprolol group. Respective figures for the placebo group were 19.4 +/- 7.9 versus 27.9 +/- 10.9 (p < 0.05), 38.5 +/- 13.0 versus 42.1 +/- 11.0 (p > 0.05), and 50.6 +/- 5.7 versus 35.5 +/- 11.7 (p < 0.05). Fractional shortening of the chords analyzed was similar in both groups during the control period; it fell significantly at the end of the experiment in three chords of the metoprolol group and in five chords of the placebo group. The apical chord in the placebo, but not in the metoprolol, dogs was dyskinetic: fractional shortening was -0.86 +/- 9.7 versus 7.5 +/- 13.5% (p > 0.05). The area at risk was 41.6 +/- 10.6 cm2 in metoprolol- and 40.5 +/- 7.2 cm2 in placebo-treated dogs (p > 0.05); the infarct size, expressed as a percentage of the area at risk, was 29.0 +/- 22.5% and 45.3 +/- 23.6% (p = 0.02), respectively. CONCLUSIONS: Oral pretreatment with metoprolol limited infarct size and improved regional left ventricular function, probably due to its negative chronotropic and inotropic effects, and also due to an enhancement of collateral flow fr

Administration, Oral↗
PubMed1994

Early intravenous administration of metoprolol enhances myocardial salvage by thrombolysis with recombinant tissue-type plasminogen activator after thrombotic coronary artery occlusion in the dog by improvement of the collateral blood flow to the area at risk.

OBJECTIVES: We studied the effects of beta 1-adrenergic blockade preceding thrombolysis on hemodynamic variables, myocardial blood flow and infarct size in a canine model of thrombotic occlusion of the left anterior descending coronary artery. BACKGROUND: Previous work suggested a reduction in infarct size and improvement in left ventricular function by intravenous beta-blockade preceding thrombolysis. METHODS: Experiments were conducted in 34 anesthetized dogs; 17 received 0.975 mg/kg body weight of metoprolol intravenously starting 15 min after occlusion, and thrombolysis was initiated 60 min after occlusion. Seventeen dogs received saline solution followed by thrombolysis. Coronary blood flow was measured by radioactive microspheres, infarct size by a dye method, hemodynamic variables by catheter-tipped pressure transducers and cardiac output by the thermodilution method. RESULTS: Infarct size in metoprolol- and placebo-treated dogs was 23.62 +/- 18.04% and 41.50 +/- 16.03% of area at risk, respectively (p < 0.01). Before occlusion, myocardial blood flow and hemodynamic variables were similar. Sixty minutes after occlusion, cardiac output (1.94 +/- 0.41 vs. 2.32 +/- 0.68 liters/min, p < 0.01) was lower in the metoprolol-treated dogs. Collateral flow to the area at risk (17.27 +/- 7.44 vs. 10.25 +/- 5.33) and to its epicardial (21.68 +/- 8.04 vs. 11.5 +/- 6.10), midmyocardial (14.30 +/- 8.63 vs. 7.35 +/- 4.94) and endocardial (13.18 +/- 8.21 vs. 6.26 +/- 5.34 cm3/min per 100 g) layers was higher (p < or = 0.05) in the metoprolol-treated dogs. The ratio of epicardial flow area at risk/circumflex territory was inversely correlated to infarct size (r = -0.69, p < 0.01). After 5 min of occlusion, collateral flow was comparable in the five dogs of each group; over the next 55 min it remained constant in the metoprolol group but decreased in the placebo dogs. CONCLUSIONS: Intravenous metoprolol, administered before thrombolysis, enhances infarct size limitation, partly by improvement of collateral flow to area at risk.

Animals↗
PubMed1994

Intravenous metoprolol preceding thrombolysis in acute thrombotic myocardial infarction in the dog; effects on infarct size, myocardial blood flow, and left ventricular function.

Intravenous (i.v.) metoprolol preceding thrombolysis in an anesthetized dog model of thrombotic occlusion of the anterior descending coronary artery helps limit infarct size (IS). We wished to determine whether these effects are caused at least in part by enhancement of collateral blood flow to the area at risk (AAR). Thrombotic occlusion was provoked by a copper-coil technique. We measured intracardiac pressures and their derivatives by catheter-tip micromanometers, cardiac output (CO) by thermodilution method, regional myocardial blood flow (RMBF) by radioactive microspheres technique, global and regional left ventricular (LV) function by ventriculography, and IS with triphenyltetrazolium at the end of the experiment. Measurements were performed before and after 60-min occlusion and after 30- and 90-min reperfusion. Received fifteen minutes after occlusion, 12 dogs metoprolol 0.3 mg/kg i.v. followed by 0.3 mg/kg/h; 12 received saline. Thrombolysis was performed in all dogs after 60-min occlusion with recombinant tissue-type plasminogen activator (rt-PA) 10 micrograms/kg/min for 30 min. Hemodynamic findings were similar in both groups. During occlusion, collateral flow to total AAR (18.6 +/- 7.5 vs. 11.0 +/- 6.1 ml/min/100 g), to its subepicardial (22.1 +/- 8.1 vs. 12.2 +/- 7.2 ml/min/100 g), midmyocardial (16.0 +/- 8.9 vs. 8.0 +/- 5.5 ml/min/100 g), and endocardial (14.1 +/- 8.1 vs. 7.3 +/- 6.0 ml/min/100 g) layers was higher (p < or = 0.03) in metoprolol than in placebo-treated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Respiratory-related blood pressure variability in patients after heart transplantation.

Our objective was to study whether the variations of blood pressure synchronous with respiration depend on the simultaneous changes of heart rate. Power spectral analysis of the heart period or R-R interval, blood pressure, and respiratory activity was performed by fast Fourier transform during 30 min of supine rest in 12 patients between 16 and 23 days after orthotopic heart transplantation and in 12 age- and sex-matched normal control subjects. The components of the variations of the R-R interval and blood pressure associated with respiration [high-frequency (HF) components] were derived from the power spectra. The HF component of the power spectrum of the R-R interval was almost absent in the transplanted patients compared with the control subjects (2.9 vs. 104 ms2; P < 0.001), whereas the HF component of the power spectrum of blood pressure was not significantly different between the two groups (1.72 vs. 1.65 mmHg2 for systolic and 0.35 vs. 0.60 mmHg2 for diastolic blood pressure). Respiratory variations of both systolic and diastolic blood pressure in humans can depend only slightly on the respiratory heart rate variations.

Blood Pressure↗
PubMed1994

Theophylline alters distribution of blood flow to respiratory muscles.

This study was designed to examine the effects of theophylline on respiratory muscle blood flow in 11 lightly anesthetized and spontaneously breathing dogs using the radioactive microsphere tracer technique. During quiet breathing, blood flow to the costal diaphragm (25.1 +/- 13.9 ml/100 g/min) exceeded blood flow to the parasternal intercostals (18.0 +/- 10.2 ml/100 g/min, p < 0.05). Inspiratory resistive loading abolished these differences by increasing blood flow to the parasternal intercostals more than to the diaphragm. Aminophylline (40 mg/kg) significantly increased minute ventilation and tidal transdiaphragmatic pressure (Pdi) swing during quiet breathing but not during inspiratory resistive loading. Theophylline did not affect diaphragmatic blood flow during inspiratory resistive loading while the same Pdi swing and tension-time index (TTdi) were reached. During quiet breathing, however, theophylline significantly (p < 0.05) increased blood flow to the triangularis sterni from 7.9 +/- 5.6 to 18.1 +/- 25.6 ml/100 g/min and to the transversus abdominis from 10.8 +/- 8.4 to 14.6 +/- 10.5 ml/100 g/min and tended to increase blood flow to the costal diaphragm and the parasternals. We conclude that (1) during quiet breathing, but not during inspiratory resistive loading, blood flow to the costal diaphragm exceeded flow to the parasternal intercostals; (2) during quiet breathing, theophylline increased blood flow to the expiratory muscles as it promoted recruitment of expiratory muscles; and (3) theophylline did not affect diaphragmatic blood flow for a given TTdi.

Airway Resistance↗
PubMed1994

Cardiac transplantation in giant cell myocarditis. A case report.

The present report describes a 15-year-old boy who underwent an urgent cardiac transplantation for giant cell myocarditis because of fulminant progressive heart failure, complicated by ventricular tachycardia, unresponsive to classical inotropic medical treatment. The physiopathology and the treatment are discussed.

Adolescent↗
PubMed1993

Experimental validation of a new quantitative method for the analysis of infarct size by cardiac perfusion tomography (SPECT).

Using global constraints and dynamic programming, a new model-based segmentation algorithm was developed to determine myocardial borders and basal plane. The segmented image is transformed to a countrate polar map and the infarct size (I.S.) is determined by comparison with a reference polar map. In order to evaluate our method the algorithm was applied to heart phantoms, to software simulations and to animal studies. In the last experiments, Tc-99m Sestamibi was used as a perfusion agent. The total myocardial volume and infarct size of a Jasczack phantom were overestimated, especially when I.S. was expressed in absolute rather than relative values. It was proven by software simulations of cardiac Spect studies that those errors were mainly due to finite resolution effects causing a clear overestimation of myocardial thickness. Implementation of a constant thickness in the algorithm resulted in a much better correlation with actual values. In a dog experiment the size of total myocardial volume of the area at risk during occlusion and of the final infarct size after thrombolysis was correlated with the histologic values obtained by planimetry after TTC staining. In 8 studies, an excellent correlation between the histologic area at risk versus the estimated perfusion defects was obtained (r = 0.97). The automatic delineation of myocardial borders and valve plane was excellent even when perfusion defects were present. Manual intervention was only necessary in certain slices where a clear overlap between liver and myocardium was present in the dog studies. Segmental polar maps expressing count rate and volume information provided a visual and quantitative tool to evaluate the influence of thrombolysis in acute ligation experiments. It is concluded that the new algorithm is ready to be used in a clinical environment for the quantitative evaluation of perfusion defects after acute myocardial infarction and for the follow-up of the therapeutic strategy.

Animals↗
PubMed1992

Isolated single coronary artery: a review of 50,000 consecutive coronary angiographies.

Single coronary artery is a rare congenital anomaly of the coronary arteries where only one coronary artery arises from the aortic trunk by a single coronary ostium, supplying the entire heart. A database consisting of the angiographic reports of 50,000 consecutive coronary angiographies performed in adult patients in the University Hospital of Leuven between March 1973 and August 1991 was searched for the diagnosis of single coronary artery. All films concerned were reviewed and classified according to their anatomical type. Thirty-three cases of single coronary artery were retrieved, yielding an incidence of 0.066%. Patient characteristics and clinical data are described, with a discussion on the pathological importance of this finding.

Adult↗
PubMed1991

Ridogrel in the setting of percutaneous transluminal coronary angioplasty.

The safety of the combination of heparin and ridogrel therapy and its antiplatelet efficacy was examined in the setting of percutaneous transluminal coronary angioplasty (PTCA). In 32 patients without known aspirin intake for 10 days before PTCA, therapy with ridogrel (300-mg intravenous bolus) was begun just before PTCA and continued orally at a dose of 300 mg twice daily until discharge. Heparin was administered as a 10,000 IU bolus dose before PTCA and followed by an intravenous infusion at a rate of 1,000 IU/hour for 24 hours. Bleeding problems at the arterial entry site occurred in 13 patients, which required a blood transfusion in only 2 patients. One patient underwent emergency bypass surgery without specific problems of hemostasis. Ridogrel virtually eliminated thromboxane B2 from the serum (29,990 +/- 6,555 pg/0.1 ml before vs 63 +/- 7 pg/0.1 ml at 2 hours after ridogrel), with a concomitant increase in serum 6-keto-prostaglandin F1 alpha (511 +/- 34 pg/0.1 ml before vs 1,190 +/- 146 pg/0.1 ml at 24 hours after ridogrel). There were no acute reocclusions in the ridogrel-treated patients, whereas acute reocclusions occurred in 5.6% of the patients taking the standard aspirin + heparin regimen during the same period. Furthermore, at 6-month clinical follow-up patients treated with ridogrel compared favorably with those receiving standard treatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Effect of superoxide dismutase on infarct size and postischemic recovery of myocardial contractility and metabolism in dogs.

The effects of superoxide dismutase treatment on infarct size, postischemic recovery of contractile function and tissue content of high energy phosphates were examined in a canine model of myocardial ischemia and reperfusion. Ischemia was induced by thrombotic occlusion of a coronary artery and reperfusion was achieved by intravenous thrombolysis. Average duration of ischemia was 90 min. Fifty closed chest anesthetized dogs were randomized to receive either superoxide dismutase (34,000 IU/min intravenously) or placebo, starting approximately 30 min before and continuing for 30 min into the reperfusion phase. Left ventricular ejection fraction and regional segmental shortening of the postischemic area were calculated from contrast angiograms after 4 h, 48 h and 1 week of reperfusion. Tissue content of high energy phosphates was determined from transmural biopsy after 4 h and 1 week. Infarct size was measured by planimetry of dye-stained heart slices. In the superoxide dismutase and placebo-treated groups, respectively, the mortality rate was 25% and 16%, collateral flow 20 +/- 10 and 23 +/- 18 ml/min per 100 g, area at risk 25 +/- 6% and 26 +/- 7% of the left ventricle and infarct size 28 +/- 19% and 36 +/- 27% of the area at risk. Multiple regression analysis failed to show any beneficial effect of superoxide dismutase treatment on infarct size. Left ventricular ejection fraction, regional segmental shortening of the postischemic area and tissue content of high energy phosphates recovered to a similar extent and at a similar rate in both treated and placebo groups up to 1 week after reperfusion. Thus, in this model of coronary occlusion and reperfusion superoxide dismutase treatment is of no benefit.

Adenosine Triphosphate↗
PubMed1991

Occurrence of lymphoproliferative disorders in heart transplant recipients.

Lymphoproliferative diseases may occur as a complication of severe immunosuppression. In our own center two out of 46 heart transplant recipients, receiving a cyclosporin A containing immunosuppressive regimen, presented with this complication and are reported here. Hepatic involvement and an occult small bowel localisation, which only became evident after a chemotherapy-induced small bowel perforation, illustrate the predilection of posttransplant lymphoproliferations for extranodal sites. Both cases represent the extremes of a spectrum of post-transplant lymphoproliferations ranging from polyclonal benign lesions to monoclonal malignant lymphomas. Their B-cell origin was pathologically established, but in none of the two reported cases the previously postulated role of Epstein-Barr virus in the pathogenesis could be confirmed by serological tests. Severe immunosuppression played a major role in the pathogenesis of these disorders, as suggested by concomitant opportunistic infections occurring in both cases. The lymphoproliferation diagnosed in the polyclonal stage was reversible after reduction of the immunosuppressive therapy, without subsequent graft rejection. This observation underscores the importance of early recognition of lympho-proliferative disorders in organ transplant patients, allowing a prompt and successful reduction of the immunosuppressive therapy. Overwhelming opportunistic infections, occurring in the patient treated with cytotoxic drugs, illustrate the inherent risks of such an approach in an already severely immunosuppressed population.

Chemical and Drug Induced Liver Injury↗
PubMed1991

Crosstalk with external bipolar DVI pacing: a case report.

An increase of the basic atrial pacing rate from a preset value of 70 beats/min up to 91 beats/min was recorded in a patient with an external bipolar dual chamber pacing system. This observation could be explained by the occurrence of crosstalk; this specific manifestation of crosstalk was the result of the use of an uncommitted DVI pacing mode.

Cardiac Pacing, Artificial↗
PubMed1990

Comparison of angiographic methods for the assessment of the extent of experimental anterior myocardial infarction in dog hearts.

Infarction was provoked in the dog by introducing a copper coil into the left anterior descending coronary artery. Eight groups, each of 6 dogs, were studied which received various treatments and were evaluated after 24 hours or 1 week. The anatomical extent of infarction was measured by the triphenyltetrazoliumhydrochloride method; size was evaluated angiographically by the centerline, chord and radial method and by ejection fraction. The extent of infarction was similar in groups studied after 24 hours and 1 week. Angiographical changes were most marked after 24 hours, and the ejection fraction was related to the extent of infarction (r = -0.5; P less than 0.02). Some parameters of the radial and centerline method showed also a relation to the extent of infarction (r = 0.47 to 0.57; P less than 0.05). After one week, the ejection fraction was no longer correlated to the extent of infarction. The correlation between the parameters of the chord, radius and centerline method and the extent of infarction improved to r-values of 0.58 to 0.63 (P less than or equal to 0.01). There was no difference between the 3 methods.

Adrenergic beta-Antagonists↗
PubMed1990

Evaluation of the effect of thrombolytic treatment on infarct size and left ventricular function by enzymatic, scintigraphic, and angiographic methods. The European Cooperative Study Group for Recombinant Tissue Type Plasminogen Activator.

In a double-blind trial of the European Cooperative Study Group, 721 patients with acute myocardial infarction of less than 5 hours' duration were given either 100 mg recombinant tissue-type plasminogen activator (rt-PA) intravenously over 3 hours or an equivalent placebo infusion. In a subset of 312 patients, infarct size was assessed by the cumulative myocardial release of alpha-hydroxybutyrate dehydrogenase (HBDH) during the first 72 hours and by planar thallium scintigraphy (index of hypoperfusion) performed 10 to 22 days after the acute event. Left ventricular ejection fraction (LVEF) was determined by contrast and nuclear angiography. The median values of HBDH during the first 72 hours were 20% lower and the median values of thallium-201 28% smaller in the rt-PA group in comparison with controls. A significant but limited improvement of angiographic LVEF (2 absolute percentage points) was also shown in the patients treated with rt-PA. A moderate but statistically significant linear association between both measurements of infarct size and LVEF was found.

Adult↗
PubMed1990

Evidence for decreased coronary flow reserve in viable postischemic myocardium.

To try to unravel the complexity and heterogeneity of the "no-reflow" phenomenon and its underlying mechanisms, we studied tissue perfusion in reperfused heart muscle by using tracer microspheres in an anesthetized dog model of 90-minute coronary occlusion followed by reperfusion for 2 1/2 hours, 24 hours, or 1 week. Regional myocardial blood flow was determined both in basal flow conditions and during reactive hyperemia. The effect of intracoronary adenosine administration was examined, and the ultrastructure of postischemic myocardium was analyzed. In viable reperfused tissue (as delineated by triphenyltetrazolium chloride staining), reflow in basal conditions is unimpaired. Coronary flow reserve (as approximated by peak reactive hyperemic flow) is intact at the start of reperfusion, decreases by more than half after 2 1/2 hours, and recovers completely within 1 week. This impairment of coronary reserve can be relieved by intracoronary adenosine administration. On ultrastructural examination, the capillaries are patent. On the other hand, in irreversibly damaged myocardium, both the basal reflow impairment and the decrease in coronary flow reserve are severe and permanent. Coronary flow reserve is already decreased at the start of reperfusion, and the pharmacological intervention has no beneficial effect. Ultrastructurally, extracellular and intracellular edema invariably are present, whereas the vascular endothelium is damaged and the capillaries are packed with red blood cells. We conclude that the no-reflow phenomenon (i.e., mechanical obstruction to blood flow) is limited to infarcted tissue. In viable myocardium, however, coronary flow reserve is transiently diminished, probably because of washout and subsequent insufficient availability of the chemical mediator adenosine after breakdown and slow recovery of the precursor ATP pool.

Adenosine↗
PubMed1989

Effect of intravenous diltiazem on myocardial ischemia occurring during percutaneous transluminal coronary angioplasty.

To investigate the antiischemic efficacy of intravenously administered diltiazem, 42 patients were randomly allocated to receive placebo or active treatment before 1-vessel percutaneous transluminal coronary angioplasty (PTCA). The development of myocardial ischemia was studied using subjective (pain) and objective (electrocardiography) parameters. Pretreatment with intravenous diltiazem resulted in a significantly delayed onset of ischemic pain and ST-segment elevation; these variables also returned to baseline earlier after balloon deflation. Thus, intravenous diltiazem prevents or delays the onset of myocardial ischemia during repetitive transient coronary occlusions; improvement of the myocardial blood flow distal to the coronary occlusion or impedance of calcium entry into the ischemic cell are considered as possible mechanisms. Because PTCA is increasingly used in patients with poor left ventricular function and more extensive disease, and because recent evidence suggests that better PTCA results could be obtained by the use of longer inflation times, the addition of diltiazem to the classic armamentarium could be beneficial.

Angina Pectoris↗