Biomedical subjects

A Hagendorff

Publications and source records attributed to A Hagendorff.

At least 55 records · Page 3Linked to original sources

PubMed1997

Confirmation of CT criteria to distinguish pathophysiologic subtypes of cerebral infarction.

PURPOSE: To determine whether cerebral infarctions classified as embolic or hemodynamic by their appearance on CT scans reflect distinct pathophysiologic entities. METHODS: Cerebral infarctions were retrospectively classified into two groups according to their morphologic appearance on CT scans: territorial infarctions and watershed, or terminal supply area, infarctions. Specific CO2 reactivity for both groups of patients was determined with the xenon-133 method and 32 stationary detectors. Twenty-one patients with unilateral, supratentorial, ischemic cerebral infarctions were selected. CT findings were highly suggestive of a territorial infarction in 14 patients (mean age, 56 years) and of a watershed infarction in seven patients (mean age, 52 years). RESULTS: The initial slope index of the territorial and watershed infarction groups during CO2 inhalation was 55.1 +/- 2.4 sec-1 and 52.0 +/- 1.9 sec-1, respectively, in the infarcted hemispheres and 58.3 +/- 2.3 sec-1 and 55.1 +/- 1.5 sec-1, respectively, in the noninfarcted hemispheres. CO2 reactivity of the unaffected detectors was 1.75 +/- 0.3 sec-1 mm Hg-1 and 1.51 +/- 0.2 sec-1 mm Hg-1 for the territorial and watershed infarction groups, respectively. CO2 reactivity of the affected detectors was 1.75 +/- 0.3 sec-1 mm Hg-1 and 1.27 +/- 0.2 sec-1 mm Hg-1 for the two groups, respectively. The CO2 reactivity difference between affected detectors of the hemodynamic group and age-matched healthy control subjects was significant. CONCLUSIONS: The difference in CO2 reactivity between the two groups supports the concept that CT criteria can identify two pathophysiologic entities. In addition, we conclude that during the chronic stage, lower CO2 reactivity of the watershed infarction indicates that the global hemodynamic situation in these infarcts is more severely compromised than in territorial infarctions.

Aged↗

PubMed1996

[Recurrent arterial thromboembolism in hereditary hypoplasminogenaemia].

HISTORY: A 26-year-old man sustained a wasp bite 5 years ago which caused arterial embolism to the right brachial artery. Now he again had a wasp bite with allergic reaction and an arterial embolus to the left brachial artery. 2 days later, after embolectomy and heparinisation, he had a cerebrovascular accident due to an embolus to the left internal carotid artery. 15 days later, despite oral anticoagulation (Quick value 10%), he had an embolism to the left femoral artery. INVESTIGATIONS: The source of the emboli was found by echocardiography to be a spherical floating thrombus on the aortic valve. The plasminogen level was only 45-61%. His mother and sister also had a low plasminogen level, i.e. he had congenital plasminogen deficiency. TREATMENT AND COURSE: At surgery, when the thrombus had been removed, a slit-like defect was found on one of the aortic leaflets and covered with a pericardial patch. At first heparin then phenprocoumon were administered, plus 250 mg ticlopidine twice daily. There have been no further complications. CONCLUSION: As the patient's fibrinolysis activity was normal, additional, probably allergic, factors must have been present to disturb the equilibrium between thrombogenesis and fibrinolysis thus causing thrombosis at a predisposed site.

Adult↗

PubMed1996

Influence of captopril on nitroglycerin-mediated vasodilation and development of nitrate tolerance in arterial and venous circulation.

We investigated whether captopril is able to potentiate vasodilation and prevent tolerance to a 48-hour infusion of nitroglycerin (NTG). Twenty-six patients were randomly assigned to a 7-day regimen of captopril (50 mg/day) or placebo. The hemodynamic response to a 0.8 mg sublingual NTG dose was assessed by measuring mean arterial pressure (MAP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), and cardiac output (CO), and calculating systemic (SVR) and pulmonary vascular resistances (PVR). The parameters were obtained serially at baseline and 1 to 10 minutes after the sublingual NTG application (day 1). Then intravenous NTG was started and maintained for 48 hours (1.5 micrograms/kg/min), and the hemodynamic study was repeated (day 3). There was no difference between the captopril and the placebo groups at day 1 (baseline values and response to sublingual NTG). After the 48-hour infusion, there was a complete loss of the NTG effects in the placebo group (day 1 vs day 3: PAP, 20 +/- 5 mm Hg vs 21 +/- 8 mm Hg; MAP, 86 +/- 11 mm Hg vs 90 +/- 9 mm Hg; SVR, 1295 +/- 330 mm Hg vs 1380 +/- 465 dyne.sec.cm-5) whereas there was still evidence of a persistent vasodilation in the captopril group (day 1 vs day 3: PAP, 19 +/- 4 mm Hg vs 13 +/- 4 mm Hg; MAP, 84 +/- 9 mm Hg vs 74 +/- 10 mm Hg; SVR, 1265 +/- 280 mm Hg vs 1140 +/- 425 dyne.sec.cm-5). The response to sublingual NTG on day 3 was markedly attenuated in the placebo group only. We conclude that captopril does not increase the vasodilatory response to nitroglycerin but is able to prevent developing nitrate tolerance in arterial and venous circulation.

Administration, Sublingual↗

PubMed1996

Relation between symptoms and profiles of coronary artery blood flow velocities in patients with aortic valve stenosis: a study using transoesophageal Doppler echocardiography.

OBJECTIVE: To analyse profiles of coronary artery flow velocity at rest in patients with aortic stenosis and to determine whether changes of the coronary artery flow velocities are related to symptoms in patients with aortic stenosis. DESIGN: A prospective study investigating the significance of aortic valve area, pressure gradient across the aortic valve, systolic left ventricular wall stress index, ejection fraction, and left ventricular mass index in the coronary flow velocity profile of aortic stenosis; and comparing flow velocity profiles between symptomatic and asymptomatic patients with aortic stenosis using transoesophageal Doppler echocardiography to obtain coronary artery flow velocities of the left anterior descending coronary artery. SETTING: Tertiary referral cardiac centre. PATIENTS: Fifty eight patients with aortic stenosis and 15 controls with normal coronary arteries. RESULTS: Adequate recordings of the profile of coronary artery flow velocities were obtained in 46 patients (79%). Left ventricular wall stress was the only significant haemodynamic variable for determining peak systolic velocity (r = -0.83, F = 88.5, P < 0.001). The pressure gradient across the aortic valve was the only contributor for explaining peak diastolic velocity (r = 0.56, F = 20.9, P < 0.001). Controls and asymptomatic patients with aortic stenosis (n = 12) did not differ for peak systolic velocity [32.8 (SEM 9.7) v 27.0 (8.7) cm/s, NS] and peak diastolic velocity [58.3 (18.7) v 61.9 (13.5) cm/s, NS]. In contrast, patients with angina (n = 12) or syncope (n = 8) had lower peak systolic velocities and higher peak diastolic velocities than asymptomatic patients (P < 0.01). Peak systolic and diastolic velocities were -7.7 (22.5) cm/s and 81.7 (17.6) cm/s for patients with angina, and -19.5 (22.3) cm/s and 94.0 (20.9) cm/s for patients with syncope. Asymptomatic patients and patients with dyspnoea (n = 14) did not differ. CONCLUSIONS: Increased pressure gradient across the aortic valve and enhanced systolic wall stress result in characteristic changes of the profile of coronary flow velocities in patients with aortic stenosis. Decreased or reversed systolic flow velocities are compensated by enhanced diastolic flow velocities, particularly in patients with angina and syncope. This characteristic pattern of the profile of coronary artery flow velocities in patients with angina or syncope may be useful for differentiating those patients from asymptomatic patients.

Aged↗

PubMed1996

Valvular aortic stenosis: risk of syncope.

BACKGROUND AND AIMS: Syncope is a serious complication of aortic stenosis. The aim of this study was to determine whether hemodynamic parameters are useful for estimating the risk of syncope in aortic stenosis. METHODS: In 43 patients with aortic stenosis, cardiac catheterization and echocardiography were performed to measure the pressure gradient across the aortic valve, the aortic valve area, left ventricular mass index, systolic left ventricular wall stress and peak systolic coronary artery flow velocities. Hemodynamic parameters were correlated with syncope and the accuracy of those parameters for determining the risk of syncope were assessed. RESULTS: Ten out of 43 patients experienced syncope. The highest correlation with syncope was found for systolic left ventricular wall stress (R = 0.74, p < 0.001). In descending order of correlation were peak systolic coronary artery flow velocity (R = 0.68, p = 0.002), the pressure gradient across the aortic valve (R = 0.62, p = 0.01) and the aortic valve area (R = 0.43, p = 0.03). Left ventricular mass index was not significantly correlated with syncope. Multivariate analysis revealed systolic left ventricular wall stress to be the only factor contributing to determining syncope (F-to-remove: 47.8). A discriminative value of > 225 dyn/cm-2 x 103 for left ventricular wall stress identified patients with a history of syncope with a specificity of 97% and a sensitivity of 90%. CONCLUSIONS: Syncope in aortic stenosis is closely correlated to increased left ventricular wall stress and attenuated, peak systolic coronary flow velocities. Cut off values may be used to identify patients with an increased risk of syncope.

Aged↗

PubMed1996

[Persistent dilatation of non-stenosed epicardial arteries in 24- and 48-hour nitroglycerin infusion].

UNLABELLED: It is still a matter of dispute to what extent a direct loss of nitrate mediated vasodilatation (true tolerance) contributes to the development of nitrate tolerance. Aim of this study was to assess to what extent the dilatation of non-obstructed segments of epicardial arteries is attenuated during a continuous 24- and 48-h-infusion of nitroglycerin. In a prospective, randomized and blinded study we investigated 32 patients who underwent diagnostic coronary angiography. All cardiac medication was withdrawn at least for 24 h; patients were randomized to either a 24 h NTG-infusion (group A; 0-24 h saline infusion followed by a 24 h NTG-infusion; n = 16) or a 48 h NTG-infusion (group B; 0-48 h of NTG-infusion; n = 16) in a dosage of 1.5 micrograms/ kg/min. The patients were included if 5 proximal segments of the left coronary artery showed no visible atherosclerosis. A coronary angiography was performed after 24 and 48 h respectively. The lumen diameters were measured by quantitative coronary analysis at baseline and 1 and 3 min after application of 0.2 mg of NTG intracoronarially (i.c.). Blood samples were drawn before and after 24 and 48 h of infusions to measure hematocrit and neurohormones. In group A after 24 h of saline infusion there was a significant increase in lumen diameter from 3.14 +/- 0.17 mm at baseline to 3.51 +/- 0.11 mm (p < 0.001) and 3.60 +/- 0.21 mm (p < 0.001) after 1 and 3 min of NTG i.e. respectively. After 24 h of NTG-infusion there were no significant changes in baseline and values after further NTG i.e. In group B after 24 h of NTG-infusion no significant change in lumen diameter was detectable after NTG i.e. (3.57 +/- 0.23 mm to 3.63 +/- 0.13 mm) and the mean diameter remained unchanged after prolongation of NTG to 48 h (3.58 +/- 0.33 mm). There were no significant differences between the baseline values and the responses to i.e. NTG after 24 and 48 h of NTG infusion. Hematocrit and aldosterone levels decreased significantly after NTG-infusion but not following saline. Renin and norepinephrine remained unchanged throughout the NTG-infusion-periods. IN CONCLUSION: The vasodilatation of non-obstructed segments of epicardial arteries persists during a prolonged infusion period and there is no induction of vascular tolerance between the 24 and 48 h infusion period. These findings further support that there is a different susceptibility of arteries and veins to nitrate tolerance.

Adult↗

PubMed1995

Randomized comparison of aspirin and phenprocoumon for prevention of right-sided thromboembolic complications associated with transvenous defibrillation leads.

Death due to pulmonary embolism caused by thrombosis formation along a pacing wire has been reported in patients with antibradycardia pacemakers. The purpose of this prospective and randomized study was to evaluate the effects of prophylactically assigned aspirin (100 mg per day) or phenprocoumon (a coumarin derivative) on the incidence of right-sided thromboembolic complications associated with transvenous defibrillation leads. Multiplane transoesophageal echocardiography and pulmonary scintigraphy were performed in 62 consecutive patients immediately and 6 +/- 2 months after transvenous defibrillator implantation. Aspirin or phenprocoumon was administered to the patients in a randomized and parallel manner. By means of multiplane transoesophageal echocardiography and pulmonary scintigraphy no thromboembolic events were observed immediately after transvenous defibrillator implantation. After 6 +/- 2 months, however, multiplane transoesophageal echocardiography disclosed thrombi on the transvenous leads in 13 of 62 patients (21%) despite antithrombotic therapy. At the same time, pulmonary scintigraphy did not reveal any defects compatible with pulmonary embolism. Although thrombi occurred in only four patients treated with phenprocoumon, but in nine patients receiving aspirin, this difference was statistically insignificant. Other variables associated with the occurrence of thrombosis formation were not identified. One fatal intracranial haemorrhage occurred in the phenprocoumon group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Echocardiographic imaging of coronary sinus diverticula and middle cardiac veins in patients with preexcitation syndrome: impact on radiofrequency catheter ablation of posteroseptal accessory pathways.

To determine the value of echocardiography for identifying coronary sinus (CS) diverticula and middle cardiac veins (MCVs) in patients with posteroseptal accessory pathways (PAPs), transthoracic (TTE) and transesophageal echocardiography (TEE) were performed in 18 consecutive patients with PAP and in 15 control subjects with left lateral accessory pathway before CS angiography. The size, shape, and location of CS diverticula and MCV were described and compared to angiography. TEE and angiography were concordant for the identification of diverticula (n = 5) and agreed for depicting MCV in 22 of the 27 cases. TTE revealed 4 of 5 diverticula and identified 4 of 27 MCV (P < 0.001). Fourteen MCV but no diverticula were found in the control subject. There was no significant difference between transesophageal and angiographic measurements for the width (23.5 +/- 4.9 vs 26.8 +/- 6.6 mm) and height (13.5 +/- 3.8 vs 15.7 +/- 3.4 mm) of the diverticula, and the width (3.5 +/- 0.7 vs 3.7 +/- 0.6 mm) of MCV. TEE underestimated the length of the MCV (12.0 +/- 1.8 vs 27.2 +/- 6.0, P < 0.001). Delivery of radiofrequency energy within the neck of a diverticulum or within an MCV was successful in 5 of 5, and 6 of 13 cases in patients with PAPs, respectively. In conclusion, echocardiography was as reliable as angiography for detecting and describing CS diverticula and MCV in patients with preexcitation syndrome. Echocardiography is recommended prior to electrophysiological study because it may simplify radiofrequency catheter ablation.

Adult↗

PubMed1995

[Cerebrogenic ECG changes after severe subarachnoid hemorrhage from an internal carotid artery aneurysm--differential diagnosis of acute myocardial infarct].

ECG-changes simulating acute posterior myocardial infarction were observed in a 62-year-old woman 16 days after acute subarachnoid hemorrhage. An acute myocardial ischemia was excluded by enzyme laboratory tests and by coronary angiography. The transient ECG-changes can be explained by short-term spasms of small distal arterioles in the heart, which were affected by a derangement of autonomic function. The present case demonstrates ECG-changes in a patient with subarachnoid hemorrhage very late after the acute event. Therefore, patients with intracranial hemorrhage should have a prolonged electrocardiographical aftercare. ECG-changes in patients with subarachnoid hemorrhage were discussed as a specific parameter describing the degree of intracranial damage and as a predictive value for a poor outcome. Because of ventricular arrhythmias and the occurrence of sudden cardiac death in patients with subarachnoid hemorrhage critical care monitoring should be performed after detection of new ECG-changes.

Autonomic Nervous System↗

PubMed1995

Paraprosthetic regurgitation in aortic prostheses: determination of the hemodynamic significance by pulsed Doppler examination of the subclavian artery flow.

Paraprosthetic leaks in aortic prostheses may cause significant aortic regurgitation. Color flow Doppler echocardiography is the method of choice for detecting paraprosthetic leaks, but quantitation of regurgitation is limited by this method. This study investigated the value of pulsed Doppler of the left subclavian artery flow for assessing the hemodynamic significance of paraprosthetic regurgitation in aortic prostheses in 32 patients with, and in 77 control subjects without paraprosthetic leaks. Paraprosthetic leaks were either detected by transthoracic or transesophageal color flow echocardiography. The hemodynamic significance of paraprosthetic regurgitation was determined by means of a dichotomous angiographic classification - significant versus insignificant regurgitation. Pulsed Doppler was performed to measure the maximal diastolic and systolic velocities, and diastolic and systolic velocity-time-integrals (VTI) and their ratios in the subclavian artery flow. The accuracy of these parameters for differentiating significant versus insignificant regurgitation was assessed. Angiography revealed 13 significant and 19 insignificant forms of aortic regurgitation. In all patients, examination of the subclavian artery was feasible by pulsed Doppler. The highest correlation between Doppler derived parameters and regurgitation was calculated for the ratios of diastolic and systolic VTI (r = 0.84), diastolic VTI (r = 0.82) and ratio of diastolic and systolic velocities (r = 0.80). An increase of the ratio of diastolic and systolic VTI (> 45%) and ratio of diastolic to systolic velocity (> 0.4), and increased diastolic VTI (> 60 cm) in the subclavian artery velocity profile identified significant paraprosthetic regurgitation with a sensitivity of 94%, 75% and 87%, and specificity of 87%, 80% and 87%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗

PubMed1994

Color-coded Doppler imaging of the vena contracta as a basis for quantification of pure mitral regurgitation.

The narrowest central flow region of a jet is defined as the vena contracta. This term is applied also to the contracted zone of the Doppler color flow image of a jet at its passage through an incompetent mitral valve. The clinical applicability of measuring the size of the vena contracta by transthoracic color-coded Doppler echocardiography for estimating the severity of mitral regurgitation (MR) was evaluated. In 78 of 82 patients with angiographically proved MR, a coherent flow image across the valve was visualized. The maximal diameter in the apical long-axis view was considered as a representative value for the size of the vena contracta. In comparison with the maximal left atrial velocity pixel area, this parameter revealed higher correlations to the angiographic degree of MR and to the regurgitant volume (r = 0.94 vs 0.72, and 0.83 vs 0.71, respectively). The highest positive and negative predictive accuracies for differentiating mild-to-moderate from severe MR were determined for a diameter of 6.5 mm (88 and 96%, respectively). Because the vena contracta is directly related to the severity of MR, it is concluded that it is helpful to use this parameter instead of the maximal velocity pixel area for semiquantitative grading.

Adult↗

PubMed1994

Carotid artery stenosis and tachyarrhythmias: regional cerebral blood flow during high-rate ventricular pacing after one vessel occlusion in rats.

The aim of the present study was to investigate the effect of hypotensive tachycardias on cerebral blood flow (CBF) in the presence of significant carotid stenosis. The experiments were performed in 57 spontaneously breathing rats during arterial normoxia and normocapnia anesthetized with thiobarbital. CBF was determined with radiolabeled microspheres during control conditions (normofrequent sinus rhythm, normotension; group A; n = 15), during high-rate left ventricular pacing (660-840 ppm) at normotension (group B1; n = 13), borderline hypotension (group B2; n = 15) and severe hypotension (group B3; n = 7). In addition, CBF measurements were performed during borderline hypotension induced by hemorrhage (group C; n = 7). Global CBF was 1.09 +/- 0.29 ml g-1 min-1 in group A, 0.93 +/- 0.40 in group B1, 0.68 +/- 0.31 in group B2 (P < 0.05 vs. A), 0.42 +/- 0.16 in group B3 (P < 0.05 vs. A) and 0.83 +/- 0.2 in group C. The highest CBF values were found in the cerebellum (A; 1.43 +/- 0.5 ml g-1 min-1) and the lowest in the postocclusive tissue of the ipsilateral hemisphere (A; 0.74 +/- 0.2 ml g-1 min-1). In all groups a 15% mean CBF reduction in the right hemispherical cerebrum in comparison to the left hemisphere was observed (P < 0.01). In contrast, hemispherical CBF of the cerebellum did not differ. The CBF blood pressure relationship shifted to lower CBF values, the threshold of CBF regulation shifted to higher blood pressure values in the tissue regions distal to the occluded vessel during hypotensive tachycardias.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Time course of myocardial and cerebral blood flow during stable but hemodynamically compromising ventricular tachycardias. Laboratory investigations.

Myocardial and cerebral blood flow were determined with radiolabeled microspheres in 20 Sprague-Dawley rats during sinus rhythm and during stable but hemodynamically compromising ventricular tachycardias. In addition, in 10 animals the measurements were performed at hypotension induced by exsanguination. In controls (n = 10), myocardial and cerebral blood flow were 5.14 +/- 0.6 and 1.03 +/- 0.3 ml/g per minute, respectively. The range of myocardial blood flow values was markedly enlarged after onset of tachycardia induced by epicardial pacing. The mean values of myocardial blood flow were 5.80 +/- 1.9 ml/g per minute (n.s.) after 1 min and 7.46 +/- 3.9 ml/g per minute (n.s.) after 5 min. Cerebral blood flow, however, significantly decreased after 1 min (0.57 +/- 0.1 ml/g per minute, P < 0.01) and after 5 min (0.71 +/- 0.3 ml/per minute, P < 0.05). In contrast, 1 min after exsanguination myocardial blood flow significantly decreased (4.03 +/- 1.5 ml/g per minute, P < 0.05) and recovered after 5 min (6.06 +/- 1.2 ml/g per minute, n.s.) Cerebral blood flow was below control levels 1 min (0.70 +/- 0.2 ml/g per minute, P < 0.05) after onset of hypotension due to exsanguination and returned to normal values with the next 4 min (0.90 +/- 1 ml/g per minute, n.s.). The results suggest that stable but hemodynamically compromising ventricular tachycardias markedly affect cerebral blood flow, whereas in most cases myocardial blood flow is maintained within normal ranges, or even increases. An augmented myocardial autoregulation can be concluded from the autoregulatory index. This maintainance of regulatory ability might be due to the increase of myocardial oxygen consumption at decreased coronary perfusion pressure during tachycardias. In contrast, during hypovolemic hypotension, myocardial as well as cerebral blood flow decreased. During stable but hemodynamically compromising ventricular tachycardias, cerebral blood flow initially drops drastically and recovers slowly over the next 5 min. This finding contrasts with the results of hypovolemic and drug-induced hypotension models.

Animals↗

PubMed1994

Reduction of cerebral blood flow with induced tachycardia in rats and in patients with coronary artery disease and premature ventricular contractions.

A reduction of cerebral blood flow (CBF) was observed in experimental studies in rats immediately after the onset of parasystolic rhythm or with stable, but haemodynamically compromising, tachycardias. Based on these data and with a view to studying the effects of premature ventricular contractions (PVCs) on the cerebral circulation in humans, CBF was measured using the 133-Xenon inhalation method in 24 age matched human controls (group A1: age 58.5 +/- 6.2 years; group A2: 52.2 +/- 7.8 years) in nine coronary artery disease (CAD) patients without PVCs (B), in 11 CAD patients with frequent PVCs (> 300.h-1) (C) and in nine patients, after exclusion of CAD by angiography, also with frequent PVCs (> 300.h-1) (D). Holter monitoring was performed during the CBF measurement. CBF determined in the human control groups A1 and A2 was 79.9 +/- 9.9 ml.100 g.-1 min-1 and 81.5-13.0 ml. 100 g-1 min-1, respectively. CBF was 74.1 +/- 13.6 ml . 100 g.-1 min-1 (P = 0.267 vs A1) in group B, 65.8 +/- 11.8 ml.100 g-1 min-1 (P = 0.004 vs A1) in group C and 74.2 +/- 15.6 ml.100 g.-1 min-1 (P = 0.218 vs A2) in group D. The significant reduction of CBF in CAD patients with frequent PVCs suggests that arrhythmias have a significant impact on CBF. Non-CAD patients with frequent PVCs did not show significant CBF decreases in comparison with controls. One can hypothetize that an impairment of electrical postextrasystolic potentiation, due to premature ventricular depolarization, and hence myocardial dysfunction leads to CBF reduction in CAD patients. The CBF reduction with CAD could also reflect concomitant coronary and cerebral arteriosclerosis.

Aged↗

PubMed1994

Myocardial and cerebral hemodynamics during tachyarrhythmia-induced hypotension in the rat.

BACKGROUND: The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension. METHODS AND RESULTS: MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias. CONCLUSIONS: The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.

Animals↗

PubMed1994

[Cerebral circulation in patients with dilated cardiomyopathy and aortic valve diseases].

The present study was performed in order to investigate the effect of dilated cardiomyopathy and severe aortic valve disease on cerebral blood flow. Cerebral perfusion was determined in 39 healthy volunteers representing two control groups of different age (77.7 +/- 8.7; 79.7 +/- 8.1 ml/100 g/min), in 7 patients with dilated cardiomyopathy (64.0 +/- 4.7 ml/100 g/min), in 11 patients with severe aortic stenosis (71.1 +/- 14.8 ml/100 g/min), and in 6 patients with severe aortic regurgitation (54.6 +/- 5.8 ml/100 g/min). Regional cerebral blood flow was measured with the 133Xenon inhalation method. Cerebral blood flow in severe aortic regurgitation patients (p = 0.006) was markedly and significantly reduced versus controls, whereas in dilated cardiomyopathy patients (p = 0.197) and in patients with severe aortic stenosis (p = 0.111) cerebral blood flow was not significantly reduced. A chronic adaptation of cerebral blood flow to the profound reduction of cardiac output is assumed in dilated cardiomyopathy patients. The collapsing pulse and the maximal reduction of mean arterial blood pressure in severe aortic regurgitation patients cause the reduction of autoregulatory capacity of cerebral blood flow with subsequent decrease of brain perfusion. Measurement of cerebral blood flow appears to be suitable for evaluation of perfusion deficits due to cardiac abnormalities. It provides an additional parameter for estimating the indication of valve replacement in patients with aortic valve disease.

Adult↗

PubMed1994

[Intermittent focal cerebral ischemia in hypotension due to pacemaker syndrome].

A pacemaker syndrome manifested as transient sensoric aphasia in a 68-year-old woman with a VVI-pace-maker implanted after SA-block. The attack occurred during long-term blood pressure recording and Holter monitoring. Borderline hypotension was documented during ventricular pacing which induced a retrograde excitation of the atrium. Clinical investigations excluded any intracranial abnormality, any source of embolism or stenosis of extra- and intracranial cerebral arteries. Cerebral blood flow measurements revealed a significant increase during pacing at elevated heart rate. Therefore, a device for AV-sequential pacing was implanted and basic pacing rate was elevated. The present case report indicates that focal and not only global cerebral ischemia can be produced by an impairment of systemic hemodynamics due to hypotension and a pacemaker syndrome. Improvement of cerebral blood flow during pacing is an unexpected finding contrasting with the concept of autoregulation. In addition, pacemaker implantation should be discussed in patients with transient cerebral perfusion deficits if an improvement of cerebral blood flow is documented along with rising heart rate.

Aged↗

PubMed1993

[Effect of frequent ventricular extrasystole on brain circulation in patients with coronary heart disease].

Animal experiments using the microsphere method indicate a 8% reduction of mean cerebral blood flow during parasystolic rhythm induced by ventricular pacing in comparison to a control group with sinus rhythm. The parasystolic rhythm causes changes of systemic arterial blood pressure, which are comparable to the hemodynamic effects of frequent premature ventricular contractions. Because a reduction of cerebral blood flow induced by frequent premature ventricular beats can be assumed by the results of the laboratory investigations, cerebral blood flow was determined in a clinical study in 19 coronary artery disease patients and in 11 healthy, age-adjusted volunteers using the 133Xenon-inhalation method, in order to investigate the effect of ventricular ectopics on cerebral perfusion. Simultaneously Holter monitoring was performed during cerebral blood flow measurements. Cerebral blood flow was estimated by the initial slope index, which is calculated from the early decay of the clearance curve, and by the mean cerebral blood flow index, which is calculated by the stochastic method. Grey matter blood flow is estimated by the two-compartment analysis. Cerebral blood flow in coronary artery disease patients is reduced versus controls. The initial slope indices were 45.2 +/- 5.1 s-1 and 57.4 +/- 7.2(-1), respectively (p < 0.01). In patients with frequent ventricular ectopic activity (739/h) an additional reduction of cerebral blood flow was observed. The initial slope index was 42.6 +/- 6.3 s-1 (p < 0.01). The reduction of cerebral blood flow in coronary artery disease patients is partially due to the coincidence of coronary and cerebral artery disease. Frequent ventricular premature contractions might cause an additional reduction.

Adult↗