[Acute arterial hypertension--causes, effects and therapy].
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Biomedical subjects
Publications and source records attributed to W Motz.
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Coronary reserve plays an important role in myocardial oxygen supply. During rest, oxygen consumption is near to maximal. An increase in myocardial oxygen demand can only be covered by an increase in coronary flow by dilation of coronary vessels. The maximal achievable rise in coronary blood flow is called coronary reserve. Coronary reserve is not only enhanced in patients with coronary artery disease but also in patients with disorders of coronary microcirculation for example in arterial hypertension. The following review will deal especially with disorders of the microcirculation in arterial hypertension. The impairment of coronary reserve is a result of structural and functional alterations. Structural alterations include an increase in media wall thickness of the small coronary arteries and a reduction of coronary capillaries. Extravascular myocardial forces which determine coronary resistance include myocardial hypertrophy and qualitative changes of myocardium like interstitial and perivascular fibrosis. The role of functional alterations like endothelial related vasomotion is discussed. The renin-angiotensin system modulates the growth of the small muscle cells of the vessels and induces protooncogenes and other growth factors. Therefore the renin-angiotensin system may also play an important role in hypertensive remodeling. Hypertensive coronary microangiopathy is diagnosed by exercise stress test and ST-segment-monitoring over 24 hours to show myocardial ischemia. Also nuclear medicine technics can be used if conventional methods of showing ischemia don't work. The diagnosis is definite if the determination of coronary reserve shows that the maximal coronary blood flow is not achieved. Coronary flow can be measured by the argon-gas-method, the thermodulation-technic or by the doppler-method. Also by nuclear medicine technics (PET) the coronary flow reserve can be determined. The advantages of these methods are discussed. In experimental studies calcium-channel-blockers, ACE-inhibitors and moxonidine showed an increase in density of capillaries and also a reduction of myocardial hypertrophy, which both result in an improvement of coronary reserve. Clinical studies of our group demonstrate that coronary microangiopathy in hypertensives can be improved by calcium-channel-blockers and ACE-inhibitors after one year treatment. Beta-receptor-blockers show no clear improvement of coronary reserve. It has to be shown by further studies whether the improvement of coronary reserve is more important for prognosis than the regression of myocardial hypertrophy.
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Five thousand consecutive percutaneous transluminal coronary angioplasties (PTCA) were electively performed between January 1988 and June 1993. They were analysed for the incidence of acute coronary occlusion, its acute treatment and subsequent course. In 133 patients (2.7%) the occlusion persisted. Recanalization by repeat PTCA was attempted in all of them, but succeeded in only 68 (51%). In 65 patients recanalization was impossible. In 25 of the latter--patients with a small infarct vessel and infarction having already occurred in the vessel's supply area while the haemodynamics remained stable--conservative treatment was practised. Acute surgical revascularization was undertaken in 30 patients (23%) with a large area and/or haemodynamic instability. In all, 14 patients died (overall death rate 0.28%, death rate of patients with occlusion 11%), ten of them before operative intervention was possible.--Not all coronary artery occlusions can be treated nonsurgically. Consequently, availability of surgical intervention at the place of elective PTCA is mandatory.
A non-transmural anterior wall infarction due to a subtotal stenosis of the anterior interventricular branch occurred in a 76-year-old man. Angiocardiography 5 weeks later demonstrated an anterior wall infarct with aneurysm. The ECG showed Q waves without any R waves and elevated ST segments in leads V2-V4. Percutaneous transluminal balloon angioplasty (PTCA) of the stenosed artery supplying the infarct area was performed. Two months later the aneurysm was no longer demonstrable by laevocardiography. The ECG changes of the anterior-wall infarct completely regressed over a 5-month period. A second PTCA was later performed because the artery had re-stenosed. The patient has remained free of angina. This case illustrates that even in the presence of ECG signs of a transmural infarct and an angiographically documented ventricular aneurysm indications for recanalization of the infarct vessel by PTCA should be widely set.
Patients with arterial hypertension frequently have angina pectoris despite a normal coronary angiogram. This angina pectoris syndrome often goes along with an impaired coronary vasodilator reserve. The aim of the study was to find out whether an impaired coronary flow reserve is associated with electrographic signs of transient myocardial ischemia. Forty-three hypertensive patients not taking cardiovascular medication were studied with 24-hour Holter monitoring. Coronary blood flow and resistance were measured before and after intravenous administration of dipyridamole (0.5 mg/kg body weight). Coronary reserve was determined as the relation of coronary resistance before and after dipyridamole. For control purposes 9 normotensive subjects were studied with the same protocol. Hypertensive patients with ST-segment depressions (n = 31) had a significantly impaired coronary reserve (2.3 +/- 0.5) compared with normotensive subjects (4.9 +/- 1.0, p < 0.01). Coronary reserve in hypertensive patients without ST-segment depressions was only slightly impaired (4.0 +/- 1.8). Arterial pressure and left ventricular mass did not differ between hypertensive patients with and without ST-segment depressions. Left ventricular mass had no effect on coronary reserve. It is concluded that neither left ventricular hypertrophy nor arterial pressure were determinants for ST-segment depressions. Consequently primary functional and structural alterations on the level of the microcirculation appear to be responsible for the occurrence of transient ischemic episodes in the Holter electrocardiogram.
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In arterial hypertension, cardiac remodeling comprises myocyte hypertrophy, interstitial fibrosis, and functional and structural alterations of the coronary microcirculation. This leads to diastolic and systolic dysfunction of the left ventricle and impairment of coronary flow reserve. Consequently, antihypertensive treatment should aim at repairing hypertensive cardiac remodeling through reversing myocyte hypertrophy, restoring myocardial structure, and improving coronary flow reserve along with blood pressure normalization. Although it has been shown that regression of left ventricular hypertrophy (LVH) can be achieved by suitable antihypertensive therapy, more insight regarding the ability to repair coronary microcirculation is needed. In spontaneously hypertensive rats (SHRs), it has been shown that coronary reserve was enhanced after hydralazine administration without concomitant regression of LVH. Likewise, administration of the calcium-channel blocker felodipine led to a reversal of medial hypertrophy in coronary resistance vessels. The angiotensin-converting enzyme inhibitor lisinopril was shown to improve coronary reserve and to reserve both medial hypertrophy and myocardial fibrosis in SHRs. Increase in length density of capillaries with either nifedipine or moxonidine treatment was also found in experimental hypertension. First clinical data indicate that, after prolonged antihypertensive treatment, coronary flow reserve can be improved in hypertensive patients with microvascular disease. Further studies are warranted to elucidate whether improved coronary flow reserve after medical treatment for arterial hypertension is due to an influence of myocardial factors, such as LVH or myocardial fibrosis or to repair of the structurally remodeled microcirculation.
We analyzed the incidence and management of a vascular occlusion at the arterial puncture site following diagnostic or interventional cardiac catheterization. During the study period 26,245 cardiac catheterization procedures were performed for diagnostic (n = 18,895) or interventional (n = 7350) purposes at our institution. A total number of 35 arterial occlusions (0.13%) was identified. In the early phase of our analysis 14 patients (40%) with peripheral vascular obstruction after cardiac catheterization underwent surgical repair. Three patients (9%) could be treated conservatively. In 18 patients (51%) acute vascular occlusion could be managed by additional intravascular manipulations: 18 patients underwent successful percutaneous transluminal balloon dilatation, in nine patients in combination with intravascular thrombolysis. In three patients additional stent-implantation was necessary in the presence of a large occlusive dissection. The procedure was primarily successful in 16/18 patients. No significant complication occurred. In two patients reocclusion led to operative thrombectomy and patch reconstruction in one and to a second catheter-based approach in the other patient. Both reinterventions were successful. Thus, in experienced hands catheter-based therapy of acute arterial obstruction following diagnostic or interventional cardiac catheterization is very effective and should be considered as therapy of first choice in these patients.
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We analyzed the changing use of coronary artery bypass grafting in our institution during the years from 1985 to 1992. All clinical parameters indicating an increased perioperative risk for the surgical intervention increased during the study period (increased percentage of old patients, females, patients with severe coronary artery disease (high modified Gensini-index or triple-vessel disease), and left main stenoses). During a 2-year follow-up there was a constant proportion of patients with a good postoperative clinical result; perioperative mortality as well as global and cardiac 2-year mortality showed no significant changes. Despite an increased proportion of patients with higher perioperative risk the acute and long-term results of coronary artery bypass surgery in our study were quite satisfactory. This must be attributed to improvements in operative techniques, improved personal skills of the surgeons, and improvements in perioperative treatment and critical care.
The mechanism of directional coronary atherectomy (DCA) results from tissue removal and mechanical dilation ("Dotter" effect, balloon inflation). To estimate the concomitant contribution of dilation to lumen enlargement by DCA, we determined the amount of retrieved tissue and the change of luminal volume (computer-based quantitative coronary artery analysis) and compared both. The first 25 patients undergoing DCA in 1992 were enrolled in this study. In all cases DCA was successful (tissue removal, residual stenosis < 50%, absence of major complications). The diameter stenosis was reduced from 68 +/- 11% to 10 +/- 24% (p < 0.001). Calculated luminal volume increased from 1.04 +/- 0.46 mm to 2.9 +/- 0.64 (p < 0.001). The comparative value of the adjacent reference segment was a luminal diameter of 3.23 +/- 0.56 mm. The increase of the calculated luminal volume was 23 +/- 13 mm3. The average weight of removed tissue was 11 +/- 7 mg. The calculated "atherectomy index" (ratio of tissue volume retrieved to change in luminal volume) revealed a significant correlation between both volumina and averaged 0.502 for the whole group. The results show that the mechanical component plays an important part in the mechanism of luminal enlargement in addition to tissue removal and therefore could be a possible explanation for the high rate of restenosis after DCA, which was documented in the recently published big DCA trials.
Antihypertensive Long-term Therapy with Isradipine/Improvement of coronary flow reserve in patients with arterial and microvascular angina In patients with arterial hypertension coronary flow reserve is often impaired due to left ventricular (LV) hypertrophy and alterations of the coronary microcirculation. Experimental and clinical studies have shown that calcium channel blockers can induce regression of myocardial hypertrophy. Objective of the present study was to see whether chronic antihypertensive treatment with calcium channel blockers can improve the diminished coronary reserve in patients with arterial hypertension and microvascular angina pectoris. Fifteen hypertensive patients with microvascular angina (61 +/- 7 years, normal coronary angiogram, mild LV-hypertrophy) were treated with isradipine (CAS 75695-93-1) (5.3 +/- 0.9 mg/d) for 12 +/- 2 months. Before and after therapy (after a washout period of 1 week) coronary flow was quantitatively measured by the gas chromatographic Argon method. Coronary reserve was calculated as the quotient of coronary resistance under baseline conditions and after dipyridamole (0.5 mg/kg i.v.). Under isradipine therapy systolic blood pressure was lowered from 165 +/- 20 to 140 +/- 13 mmHg (p < 0.01) and diastolic blood pressure from 98 +/- 8 to 88 +/- 6 mmHg (p < 0.01). The LV muscle mass index decreased by 10% from 154 +/- 33 to 139 +/- 28 g/m2 (p < 0.05). Baseline coronary blood flow (81 +/- 13 versus 83 +/- 16 ml/min x 100 g, n.s.) was identical before and after therapy. There were also no differences in coronary perfusion pressure, heart rate, myocardial oxygen consumption and arterio-coronary venous oxygen difference before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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Patients with arterial hypertension often have angina pectoris and a positive exercise tolerance test, even when their epicardial coronary arteries are of normal anatomic appearance. In these patients, coronary vasodilator capacity is frequently impaired by 30-50%, predominantly owing to microvascular alterations. These include medical thickening, decreased capillary density, perivascular fibrosis, and an impaired endothelium-dependent coronary vasodilation. An antihypertensive treatment that can be considered cardioreparative restores myocardial structure through both regression of myocardial fibrosis and regression of the structural coronary microvascular alterations. We believe that this is the first clinical study to show that coronary flow reserve was considerably improved after long-term medical blood pressure normalization.
Rapid reperfusion of the occluded coronary artery is essential for the reduction of mortality and complications of acute myocardial infarctions. Intravenous thrombolytic therapy using various thrombolytic substances has proven to be effective and easy to perform and has gained widespread acceptance for treatment of acute myocardial infarction. Because of several contraindications, as well as failure to achieve patency of the infarcted vessel in 25-30% of patients, severe bleeding complications, a time interval of 6 or more hours after suspected onset of myocardial infarction, and a high rate of recurrent ischemia, this treatment is currently limited to a small percentage of patients with acute myocardial infarction. Immediate percutaneous transluminal coronary angioplasty (PTCA) can be applied to nearly every patient presenting with acute myocardial infarction. Therefore, we offer immediate PTCA as the primary treatment to all of our patients presenting with acute myocardial infarction. Between January 1987 and December 1991, immediate PTCA was performed in 785 of 903 (87%) consecutive patients (aged 23-86 years, mean 61 +/- 10). 82% (640/785) of the patients were men. Anterior myocardial infarction was present in 372 patients (47%), inferior infarction in 413 patients (53%). 245 patients (31%) had 1-vessel disease, 221 patients (28%) two-vessel disease and 319 patients (41%) had three-vessel disease. 97 patients (12%) were in cardiogenic shock. In 675/785 patients (86%) the infarct related vessel was occluded (TIMI < or = 1). 86% of patients had a patent infarct related vessel (TIMI > or = 2) leaving the catheterization laboratory. The overall in-hospital mortality was 6.9% (54/785 patients), after exclusion of high-risk patients (age > 75 years, cardiogenic shock, PTCA under cardiopulmonary resuscitation) mortality decreased to 2.5%. Recurrent ischemia necessitated immediate repeat PTCA in 4.4% of the patients, in 8.1% of patients another elective PTCA was performed during hospitalization and 9.7% of patients were sent to surgery (4.0% on an emergency basis). 87% of all patients presenting with acute myocardial infarction could be treated successfully with immediate PTCA. With respect to the severely ill group of patients the primary success rate is high, the rate of reocclusion is low, and the overall mortality is extremely low. From our data, it is obvious that immediate PTCA compared to thrombolytic therapy is the superior treatment of myocardial infarction.
The poor prognosis of arterial hypertension is mainly determined by its cardiac organ damages. Even borderline arterial hypertension significantly increases coronary morbidity and mortality, particularly in the presence of other risk factors such as hypercholesterolemia, diabetes, and cigarette smoking. Arterial hypertension causes myocardial hypertrophy and fibrosis, and affects coronary microcirculation by structural and functional changes of the small intramural resistance arteries, rarefiction of arterioles and capillaries and a distinct disturbance of endothelial vasomotion (i.e. "hypertensive remodeling"). Moreover, the presence of arterial hypertension predisposes to atherosclerotic coronary artery disease. Regarding the benefit-risk-ratio of antihypertensive therapy, benefit is much greater than risk: 1) An antihypertensive treatment with ACE-inhibitors, calcium channel blockers, beta-receptorblockers and anti-sympathicotonic substances leads to both reversal of LV hypertrophy and improvement of coronary flow reserve. Incidence of hypertensive heart failure has dropped considerably during the last 20 years. 3) Intervention studies have shown at least a clear tendency of a reduction in coronary morbidity and mortality. 4) In patients with coronary artery disease diastolic blood pressure should not be lowered under 85 mm Hg (J-curve). 5) An antihypertensive treatment should not adversely influence blood lipids when cholesterol is elevated. 6) Even in very elderly patients medical intervention to lower blood pressure is indicated from the cardiologic point of view (SHEP- and SHOP-studies).
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