Biomedical subjects
Publications and source records attributed to H De Geest.
This report describes a patient with a single coronary artery system, in whom the right coronary artery originated from the distal left circumflex. A significant stenosis was present just at the take-off of the aberrant right coronary artery. No other associated cardiac anomaly could be demonstrated; the patient was referred for elective bypass surgery.
Coronary blood flow velocity and coronary flow reserve can be assessed in humans using a coronary Doppler catheter and the vasodilator papaverine. Although it is a safe, elegant and reproducible technique, serious complications can occur. Coronary flow reserve assessment in a 49-year-old man with a critical stenosis in the proximal part of the circumflex artery was complicated by a papaverine-induced ventricular arrhythmia. Several features of the present case report support papaverine-induced disturbances of the repolarization phase as the pathophysiological mechanism: a 'torsade de pointes' pattern of the tachycardia, the lengthening of the QT-interval, the appearance of a new U-wave and the presence of additional risk factors (hypokalaemia and alcalosis). Patients presenting additional risk factors for this complication should be excluded from coronary flow reserve assessment.
Hemodynamic changes after the subselective intracoronary administration of 50 micrograms of nisoldipine were analyzed in 24 nonstenotic coronary arteries using a randomized, placebo-controlled, double-blind protocol. The following hemodynamic parameters were studied: (a) epicardial coronary artery diameter, assessed by quantitative angiography; (b) coronary blood flow velocity, measured by an intracoronary Doppler probe; (c) coronary blood flow, calculated from the above parameters; (d) coronary flow velocity reserve, assessed after intracoronary administration of 10 mg of papaverine hydrochloride; and (e) heart rate and arterial blood pressure. Since 3 patients were excluded due to unreliable Doppler signals, a total of 21 patients was eligible for complete analysis (placebo: n = 9; nisoldipine: n = 12). In placebo-treated patients, all studied parameters proved to be very stable on repeat measurement and no significant changes were found. In nisoldipine-treated patients, a significant increase in epicardial diameter (+19%; p = 0.0001) and coronary blood flow (+47%; p = 0.003) was found. The coronary blood flow velocity transiently increased after nisoldipine, with a maximum (+80%) after 2 min and returning to baseline within 10 min. Finally, nisoldipine resulted in a significant decrease in the coronary flow velocity reserve by 20% (p = 0.001). All coronary hemodynamic effects were observed in the absence of changes in heart rate and arterial blood pressure. Therefore, the present data demonstrate that nisoldipine acts as a potent dilator of epicardial as well as resistance vessels in nonstenotic human coronary arteries.
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.
The natural history of symptomatic young patients with coronary artery disease is often far from benign. Follow-up studies of young patients who have undergone coronary bypass graft surgery show frequent recurrence of symptoms and need for reoperation. Prompted by these considerations, we reviewed the records of 23 consecutive patients aged less than or equal to 35 years with symptomatic coronary artery disease, who underwent coronary balloon angioplasty at our center between August, 1984 and November, 1989. Mean patient age was 32 (3) (mean [SD]) years. Acute myocardial infarction was the first symptom of coronary artery disease in 7 (30%) of the 23 patients. At the time of angioplasty, 17 (74%) patients, had functional Class 3 or 4 anginal symptoms. Eight (35%) had multivessel coronary artery disease (stenoses greater than or equal to 70% in two or more major coronary arteries). Overall, a total of 36 critical coronary lesions were identified in 32 vessels of the 23 patients (mean of 1.6 lesions and 1.4 diseased vessels per patient). At angioplasty, dilatation of 31 lesions in 27 vessels was attempted. Multilesion angioplasty was attempted in 7 (30%) patients. Successful dilatation was achieved in 29 of the 31 (94%) lesions, and 25 of the 27 (93%) vessels. Primary clinical success (successful dilatation of all attempted lesions without any complications) was achieved in 21 of 23 (91%) patients. Three of the 21 patients with successful initial angioplasty had repeat angioplasty for restenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
A single oral dosage of 100, 200 or 300 mg Epanolol or placebo was administered in a randomized double-blind, cross-over fashion to 12 patients with stable effort angina. Symptom limited bicycle ergometer tests were performed before and 2 and 8 hours after each drug administration. Spontaneous diurnal and day to day differences in exercise tolerance and related analyzed variables were not present; 48 hours after drug intake a carry-over effect of the previous Epanolol administration could not be demonstrated. At each dose level of Epanolol, 2 hours after drug intake, heart rate and rate pressure product at peak exercise fell while exercise duration rose significantly. After 8 hours these effects were less marked. No significant differences between the 3 dose levels were found. In the pooled data of the 3 Epanolol doses, systolic blood pressure at peak exercise and maximal ischemic ST segment depression during exercise were also significantly reduced after 2 hours, while total performed external work rose. The percentage increase in heart rate during exercise after Epanolol administration was similar to the control tests at lower exercise levels but was less marked during the later stages of the test. Heart rate after Epanolol intake was percentage wise more reduced at higher exercise levels. Plasma levels of Epanolol were lower 8 hours after drug administration than after 2 hours. There was no correlation between plasma levels of Epanolol and the observed changes of any of the exercise variables 2 hours after drug intake.
Epicardial coronary artery diameter (ECAD), coronary blood flow velocity (CBFV), and coronary flow velocity reserve (CFVR) were analyzed at baseline and after a 500 micrograms i.c. bolus of diltiazem in nonstenotic coronary arteries of awake humans. Furthermore, patients (n = 25) were first randomized to pretreatment either with placebo (n = 12) or isosorbide dinitrate (0.5 micrograms/kg/min infusion) (n = 13). Diltiazem resulted in a significant increase in epicardial diameter (+10%; p = 0.001) and in coronary blood flow (CBF) (+30%; p = 0.0001). Whereas basal CBFV only slightly increased (+7%; NS), there was a significant fall in CFVR (-11%; p = 0.001). The increase in coronary diameter and CBF after administration of i.c. diltiazem was comparable in placebo- and nitrate-pretreated patients. The decrease in CFVR, however, was restricted to the placebo-pretreated patients (-21%; p = 0.0004). Apparently, diltiazem attenuated the CFVR but only in the absence of nitrates. Thus, diltiazem i.c. appears to enhance myocardial oxygen supply without deleterious effects on the distal coronary perfusion pressure.
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.
The severity of the infarct-related residual coronary stenosis after spontaneous or therapeutic thrombolysis was quantitatively assessed in 91 patients with an acute myocardial infarction who were allocated to treatment in the acute stage with either a thrombolytic agent (100 mg of recombinant tissue-type plasminogen activator given over 3 h, 49 patients) or a placebo (42 patients). Heparin and aspirin were given to both groups until angiography was performed. Digital subtracted images of the infarct-related coronary vessel were obtained 10 to 14 days after hospital admission and were subsequently analyzed with the use of a computer-assisted coronary stenosis measurement system. Neither treatment group differed significantly in age, gender or location of the culprit coronary lesion. Median values (90% range) in the thrombolysis and control groups were, respectively, 1.95 (0.9 to 5.3) mm versus 1.7 (0.9 to 3.4) mm for stenosis length; 1.4 (0.8 to 2.7) mm versus 1.4 (0.9 to 1.8) mm for minimal luminal diameter; 57% (36% to 75%) versus 58% (44% to 71%) for diameter obstruction; 82% (59% to 95%) versus 82% (68% to 92%) for geometric area obstruction; and 78% (58% to 91%) versus 79% (66% to 90%) for densitometric area obstruction. The difference between the two groups was not statistically significant for any of these measurements. Thus, in this study no significant differences in anatomy or severity of residual coronary stenosis could be demonstrated at 10 to 14 days after an acute myocardial infarction in patients with a recanalized infarct-related vessel, whether or not thrombolytic therapy was given on admission. These results indicate that with effective antithrombotic treatment, gradual endogenous fibrinolysis or more rapid lysis induced by the infusion of a thrombolytic agent results in a similar infarct-related coronary lesion at the time of hospital discharge.
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.
STUDY OBJECTIVE: The aim was to study the fate of enlarged bronchial arteries after resolution of experimental pulmonary embolism. DESIGN: Embolisation of the pulmonary arteries of both lungs was performed with intravenous gelfoam. Pulmonary pressure and pulmonary arteriolar resistance were measured 1 h, 40 d and 80 d after embolisation. Pulmonary angiography and aortography were performed at the same time to evaluate the pulmonary emboli and the collateral bronchopulmonary circulation. Aortography and gross pathological and histological examination of the lungs was performed after 80 d. EXPERIMENTAL MATERIAL: 15 adult mongrel dogs of either sex were studied, weight 22-25 kg. Nine dogs were embolised and there were six controls. MEASUREMENTS AND MAIN RESULTS: All animals survived until 80 d. There was a rise (p less than 0.001) in mean pulmonary artery pressure and arteriolar resistance 1 h after embolisation. Pulmonary artery pressures and resistances were still raised 40 d after embolisation but had returned to normal after 80 d. Pulmonary arteriography at 1 h confirmed massive thromboembolism. After 40 d antegrade pulmonary blood flow was almost completely restored, and the thromboemboli had largely disappeared. Pulmonary angiograms were completely normal after 80 d. Aortography after 40 d showed a well developed collateral bronchopulmonary circulation, most pronounced in the lower lobes, which persisted unchanged until 80 d. Aortography and gross pathological and histological examination at necropsy confirmed the presence of hypertrophic well developed bronchial arteries to both lower lobes and to a lesser extent to the middle and upper lobes, with only a few organised and recanalised thrombi in segmental arteries of both lower lobes. CONCLUSIONS: Our data show a temporal dissociation between the resolution of pulmonary thromboemboli in the present model and the eventual regression of developed bronchopulmonary collateral vessels. The mechanism of this dissociation could not be elucidated.
STUDY OBJECTIVE: The aim was to record diastolic transmitral pressure gradients at high sensitivity to quantitate the effect on transmitral pressure gradients of changing the heart rate. DESIGN: Diastolic left atrial and left ventricular pressures were recorded at high sensitivity (40 mm Hg = 10 mm recorded deflection) in control conditions (heart rate 70 beats.min-1) and after intravenous administration of atropine or isoprenaline (heart rate 110 beats.min-1). A special ventricular extrasystole protocol enabled the zero level of the transmitral pressure gradients to be unequivocally determined at high heart rates. The effect of atropine and isoprenaline on the pressure gradients, absolute diastolic pressures, and diastolic time intervals was investigated. EXPERIMENTAL MATERIAL: 16 mongrel dogs, 16-25 kg, were used. MEASUREMENTS AND RESULTS: Below a heart rate of 110 beats.min-1, four distinct periods were identified, during which a pressure gradient existed. During early and late diastole, a positive pressure gradient was consistently followed by a negative pressure gradient. Mean negative pressure gradient during early diastole correlated with the pressure difference of rapid filling wave (r = 0.72, p less than 0.01) and with mean positive pressure gradient during early diastole (r = 0.66, p less than 0.01). At a heart rate of 110 beats.min-1, isoprenaline augmented, while atropine reduced, the mean positive pressure gradient during early diastole without affecting the time interval over which the gradient occurred. This divergent action of the two drugs was related to their different effects on the decay of left ventricular pressure, which fell faster and deeper with isoprenaline but not with atropine. Both drugs shortened the time interval of the negative pressure gradient in early diastole without significantly affecting the mean negative pressure gradient during this period. In late diastole, atropine augmented the mean positive pressure gradient more than isoprenaline, reflecting the higher afterload after administration of atropine. Neither drug affected the time interval of the positive pressure gradient. As a result of a shortening of the P-R interval, isoprenaline shortened the time interval of the negative pressure gradient and reduced its mean value. Such an effect was not observed with the dose of atropine used. CONCLUSIONS: We conclude that a pressure gradient reversal in early diastole is always observed below a heart rate of 110 beats.min-1 and that isoprenaline and atropine affect the pattern of transmitral pressure gradients in a different way.
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.
Between April 1988 and October 1989, 22 adult patients with isolated or predominant severe mitral stenosis underwent Percutaneous Transvenous Mitral Valvuloplasty (PTMV). In 20 patients, a transseptal double balloon technique was used; in the last 2 patients, dilatation was performed using the Inoué balloon. Immediately after the procedure, the mitral valve area (MVA) rose from 1.2 +/- 0.3 to 2.2 +/- 0.8 cm2 (p less than 0.0001) using the hemodynamic method and from 1.1 +/- 0.4 to 1.9 +/- 0.4 cm2 (p less than 0.0001) using a Doppler technique. The mean left atrial pressure decreased from 20.3 +/- 6.0 to 10.5 +/- 5.0 mm Hg (p less than 0.0001). After the procedure, severe mitral regurgitation or significant iatrogenic interatrial septum defect did not occur. Two cerebral accidents were observed. One patient had a severe stroke with aphasia and hemiplegia but recovered within 3 months. The other patient had a minor dysarthric event, which resolved completely after 24 hours. Three months follow-up data in 16 patients revealed that they all were in NYHA class I or II. Restenosis occurred in 1 case. In the whole group of patients the MVA calculated by Doppler examination was similar to immediately after PTMV (1.9 +/- 0.4 versus 1.9 +/- 0.7 cm2).
A questionnaire was administered to 338 cardiac patients susceptible to infective endocarditis seen at the outpatient clinic or a cardiac ward. The questionnaire consisted of a series of questions on the educational, social, familial and professional background, the medical and dental history and the knowledge of the patient on prophylaxis of infective endocarditis. Univariate analysis (chi-square test) and stepwise discriminant analysis were used to evaluate the factors responsible for the presence or absence of an acceptable degree of awareness of infective endocarditis. More than half of the patients had no knowledge on prophylactic measures. The time since the diagnosis of heart disease, an edentulous state, written instructions received in the past on prophylaxis, the location of the follow-up, the level of education and previous prosthetic valve surgery were factors retained by discriminant analysis. A discriminant score was calculated for each patient and permitted classification in subgroups with a high, intermediate and low probability of presence of knowledge. This was simplified by classifying patients according to the number of risk factors. An answer to one of the six variables, selected by discriminant analysis, unfavorable for the presence of knowledge, was considered as a risk factor. Risk factor analysis must be considered as an important tool in the education of patients on the risk and prophylaxis of infective endocarditis.
Three hundred and thirty-eight cardiac patients, at risk of infective endocarditis, filled in a questionnaire consisting of a series of questions on their social, educational, familial, professional, medical and dental history and also on their level of dental care. Univariate (chi-square test) and stepwise discriminant analysis were applied to evaluate the factors related to or responsible for the presence or absence of a sufficient level of dental care, defined as at least one dentist visit per year and once daily teeth brushing. An acceptable level of dental care was present in one third of the dentate but almost nonexistent in edentulous patients. Univariate analysis revealed that in dentate patients level of education, knowledge of endocarditis prophylaxis, previous cardiac surgery, time since first heart operation and type of previous operation (artificial valve surgery) were significantly related to the level of dental care. Level of education, knowledge of endocarditis prophylaxis and time since first heart operation were withheld as independent factors by discriminant analysis. A discriminant score was calculated for each patient which permitted classification of the patients in two groups: one with a very high chance for absence of appropriate dental care and one with an equal chance for sufficient or insufficient care. Patients were also classified according to the number of risk factors. An answer to one of the 3 variables, selected by discriminant analysis, unfavorable to the presence of sufficient dental care, was considered a risk factor. Patients with two risk factors had a very high chance for the absence of sufficient dental care; in those with 0 or 1 factor, chances were divided between sufficient and insufficient dental care.
Between October 1986 and January 1989, 57 attempts of percutaneous transluminal valvuloplasty were made in 51 elderly patients, mean age 76.7 +/- 6.2 years, with symptomatic aortic stenosis; this included 3 failures and 6 repeat valvuloplasties. The procedure resulted in a significant immediate decrease of the peak-to-peak transaortic pressure gradient from 94.6 +/- 26.5 to 42.6 +/- 17.9 mm Hg (p less than 0.002) and an increase of the surface of the aortic valve from 0.4 +/- 0.1 to 0.6 +/- 0.2 cm2 (p less than 0.001). Cardiac output remained unchanged: 3.8 +/- 0.9 vs 3.8 +/- 0.8 lit/min. Complications included local vascular injury requiring surgical repair in 7 patients, cerebral events in 3 patients and disruption of the aortic annulus, the aortic wall and the pulmonary artery each in 1 patient, and resulted in 4 in-hospital deaths (8%). Follow-up data were available for all patients for a mean duration of 12.7 +/- 5.4 months. Fifteen patients (30%) died on average 9.0 +/- 4.9 months after discharge. Recurrence of symptoms and early restenosis were documented in the majority of the patients. Restenosis was successfully treated by repeat valvuloplasty in 4 and by valve replacement in 4 patients. Doppler echocardiography predicted the severity of the aortic stenosis before valvuloplasty and was very useful to assess follow-up results. Because of the limited hemodynamic results, the numerous procedural complications and the development of early restenosis balloon valvuloplasty of aortic stenosis should be restricted to selected symptomatic elderly patients.
A patient with calcified aortic valve disease secondary to ochronosis and alkaptonuria is presented. Urgent aortic valve replacement was necessary. The cardiovascular complications of this disease are reviewed.