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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with chest pain and normal epicardial coronary arteries are characterized by an impairment of myocardial perfusion reserve. Functional and morphological abnormalities of the intramyocardial arterioles are suggested to be responsible for this, possibly as a consequence of hypertension and/or left ventricular hypertrophy. In an attempt to isolate predisposing factors of microvascular angina we investigated 34 patients (15 f, 19 m) with a mean age of 53 +/- 7 years. They were diagnosed as microvascular angina without hypertension or left ventricular hypertrophy. Parameters such as plasma insulin, glucose, cholesterol, LDL-cholesterol, triglycerides, (VLDL-cholesterol) and fibrinogen were determined for a metabolic profile. Furthermore, insulin and glucose were measured after an oral glucose load of 100 g glucose (OGTT) over 3 h. All parameters were compared to a control group of 15 healthy people matched for age and body mass index. In the study population systolic blood pressure was within normal limits at 137 +/- 17 mm Hg and thus higher than control at 124 +/- 11 mm Hg (p < 0.02). Furthermore, diastolic blood pressure was 85 +/- 7 mm Hg compared to 78 +/- 9 mm Hg in controls (p < 0.02). Insulin was significantly elevated in patients with microvascular angina 90 min (median: 101 vs 54 microU/ml; p < 0.01) and 120 min (median: 88 vs 51 microU/ml; p < 0.05) after ingestion of 100 g glucose. The fasting glucose was elevated at 98 +/- 12 compared to 87 +/- 7 mg/dl in controls (p < 0.01). Glucose concentration was also elevated after 30 min at 176 +/- 28 compared to 148 +/- 32 mg/dl (p < 0.02), after 45 minutes (198 +/- 35 compared to 152 +/- 53 mg/dl) (p < 0.01) and 60 minutes (193 +/- 44 compared to 145 +/- 54 mg/dl) (p < 0.01). In microvascular angina parameters such as total cholesterol: (244 +/- 46 vs 199 +/- 29 mg/dl (p < 0.01)), LDL-cholesterol (157 +/- 41 vs 122 +/- 18 mg/dl (p < 0.01)) and fibrinogen: (377 +/- 150 vs to 285 +/- 69 mg/dl (p < 0.03)) were elevated. These findings suggest a pathogenetic role of insulin resistance, hyperlipoproteinemia and elevated levels of fibrinogen for impaired myocardial coronary reserve. This metabolic constellation as well as exhaustion of coronary reserve is often found in hypertensive patients and may identify microvascular angina as an early stage of hypertensive heart disease before manifest hypertension has developed.
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PMID:[The significance of insulin resistance and hyperlipidemia in microvascular angina (syndrome X)]. 773 10

We studied 3,942,868 Medicare patients (comprised of elderly and disabled) discharged with cardiovascular disease (CVD) during 1987, of which 41,095 (1%) had a drug disorder. Among this small subgroup, the percent of those overlapping with an alcohol and/or mental disorder is 33% for the elderly and 47% for the disabled. The presence of a drug disorder discharge diagnosis is associated with an excess of 329,650 days of hospital care and +174,498,071 in hospital charges as illustrated by a 51% increase in average annual days in the hospital for the elderly, and a similar 61% increase for the disabled. The concomitant increase in average annual discharges offers an explanation. Clinical progression in drug disorder severity (six categories were defined) is associated with increasing lengths of stay; for example, drug dependence comorbidities present longer lengths of stay than drug abuse comorbidities. Among the 12 categories of CVD defined, patients with rheumatic heart disease, hypertensive heart disease, hypertension, and other venous disorders were those whose length of stay experienced the largest percent increase when a drug disorder was present. When drug disorders compete with alcohol and/or mental disorders in a general linear model predicting average annual length of stay, they remain significant at the p < .001 level.
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PMID:Drug disorders and cardiovascular disease: the impact on annual hospital length of stay for the Medicare population. 776 47

In arterial hypertension, coronary flow reserve, expressed by the difference between autoregulated and maximal coronary flow, is frequently impaired. Previous experimental and clinical investigations using acetylcholine as a stimulus for the production of endothelium-derived relaxing factor suggested that an impaired endothelium-dependent vasodilation, presumably caused by a decreased formation of nitric oxide (NO), may account for this microvascular dysfunction. However, so far no study has been performed that quantifies the formation of NO within the coronary circulation of hypertensive hearts to assess its role in setting coronary vascular tone in the hypertensive heart. We therefore quantified NO formation within the coronary circulation of constant flow-perfused, isolated hearts from spontaneously hypertensive rats (SHR, 16th to 26th week), as a model for hypertensive heart disease, and from the normotensive control strain (Wistar-Kyoto, WKY) using the oxyhemoglobin technique. Coronary perfusion pressure and vascular resistance were almost 30% higher in SHR compared with WKY hearts. Intracoronarily applied NO decreased coronary vascular resistance by maximally 45% of resting values in a concentration-dependent manner in both groups. The bradykinin-induced decrease in coronary vascular resistance and the parallel increase in NO release were comparable in SHR and WKY hearts and fell within the vasodilator range of exogenously applied NO. Moreover, basal release of NO normalized to heart wet weight was 50% higher in SHR compared with WKY hearts. Rates of basal NO release were correlated inversely with changes in coronary perfusion pressure and vascular resistance in both groups (r = -.85 and -.84, respectively, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Feb
PMID:Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide. 784 68

The Joint National Committee Reports IV (1988) and V (1992) have emphasized individualization of drug therapy for patients with hypertension-a departure from the "stepped" care approach of initiating therapy with diuretics as advocated by the JNC I-III in the 1970's and 1980's. This review highlights individualization or "patient profiling" using calcium channel blockers as first-line treatment strategy for patients with primary hypertension--especially in the patient who has attendant risk factors and sequelae. The calcium channel antagonists, especially effective in elderly and Black patients, have proven efficacy in reducing left ventricular hypertrophy and improving diastolic function in patients with hypertensive heart disease. The heart rate limiting calcium antagonist, verapamil, has been found effective in outcome trials of reducing death and reinfarction rates post myocardial infarction and is an alternative therapy for the beta blocker intolerant hypertensive post myocardial infarction. More vascular specific dihydropyridines (felodipine, isradipine, and amlodipine) may be preferable to rate limiting agents in hypertensives with sinus node or AV conduction disorders and in those with impaired left ventricular systolic function. Verapamil and diltiazem have been effective in preliminary trials in reducing proteinuria and preserving renal function in both diabetic and non diabetic hypertensives. Calcium channel antagonists appear to prevent the progress of atherosclerosis independent of their antihypertensive properties. Further, they have theoretic value in improving endothelial mediated vasodilation.
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PMID:Individualization of therapy for hypertension in the 1990's: the role of calcium antagonists. 785 64

Myocardial fibrosis is associated with an activated renin-angiotensin-aldosterone system (RAAS). In renovascular hypertension, this presents as a reactive perivascular and interstitial fibrosis in not only the pressure overloaded, hypertrophied left ventricle but also the normotensive, nonhypertrophied right ventricle. It therefore would appear that circulating hormonal and not hemodynamic factors are responsible for this adverse fibrous tissue response. To ascertain whether the RAAS effector hormones angiotensin II (AII) or aldosterone (ALDO) directly stimulate collagen synthesis or inhibit collagenase production we used cell culture. Adult rat cardiac fibroblasts (Fb) were cultured since these cells express mRNA for types I and III collagens, the major fibrillar collagens in the heart, and collagenase or matrix metalloproteinase 1 (MMP 1), the key enzyme for interstitial collagen degradation. Collagen synthesis, determined by 3H-proline incorporation, and collagenase activity were measured in confluent, quiescent Fb after 24 h incubation with various concentrations of AII or ALDO (10(-11)-10(-6)M) in the presence or absence of either 10(-5)M type 1 (DuP 753) and type 2 (PD 123177) AII or 10(-9)-3 x 10(-6)M ALDO (spironolactone) receptor antagonists, respectively. Collagen synthesis, normalized per total protein synthesis, increased significantly (P < 0.005) after incubation with either 10(-9)M ALDO (5.9 +/- 1.0%) or 10(-7)M AII (5.3 +/- 1.2%) compared with untreated control cells (2.9 +/- 0.5%) of the same passage (p6-p10). This increase in collagen synthesis could be completely abolished by either types 1 or 2 AII receptor antagonists in AII stimulated Fb or the competitive ALDO receptor antagonist, spironolactone, at equimolar concentration in ALDO stimulated Fb. AII significantly decreased collagenase activity which could be completely abolished by PD 123177, but not DuP 753, while ALDO had no effect on collagenase activity. The mineralocorticoid, ALDO, stimulates collagen synthesis in cultured adult rat cardiac Fb in concentrations similar to those found in plasma in renovascular hypertension and this response appears to occur via type I corticoid receptors. AII appears to stimulate collagen synthesis by both type 1 and 2 AII receptors, but only in high concentrations that could be generated locally within the myocardium. In addition, AII unlike ALDO inhibits collagenase activity that could be attenuated only by type 2 receptor blockade. These findings suggest a direct interaction between ALDO, AII and cardiac Fb in mediating myocardial fibrosis in hypertensive heart disease.
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PMID:Collagen metabolism in cultured adult rat cardiac fibroblasts: response to angiotensin II and aldosterone. 796 49

Abnormalities of left ventricular diastolic function in hypertension are multifactorial in origin. Of importance is the demonstration that abnormalities of left ventricular filling in hypertension may be accompanied by deleterious cardiovascular neurodynamic regulations. However, the left ventricular filling rates can be normalized during medical treatment of hypertension. In particular, regression of left ventricular hypertrophy is almost always associated with or followed by improvement of left ventricular filling. The effects of this normalization on cardiovascular dynamics and the outcome of hypertensive heart disease are yet to be demonstrated.
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PMID:Left ventricular diastolic dysfunction in hypertension. 798 34

Individuals with hypertension and electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH) have a 10-fold greater risk of developing cardiac failure than hypertensives without ECG evidence of LVH. LVH in hypertension is characterized by myocardial fibrosis and structural changes to the small intramural arteries. Hypertensives with or without LVH have reduced coronary vasodilator reserve due to hypertensive disease of small coronary arteries. Prognosis of arterial hypertension is largely determined by cardiac complications. The aim of treatment of hypertensive heart disease is to reverse myocardial hypertrophy in order to prevent progression to hypertensive heart failure, as well as reversal of the hypertensive disease of small coronary arteries in order to improve coronary reserve. On the development of hypertensive heart failure, administration of digitalis, diuretics and angiotensin converting enzyme (ACE) inhibitors should be initiated. Although regression of LVH can be induced by dihydropyridine calcium channel blockers, ACE inhibitors and sympatholytic substances, clinical evidence of the reversal of hypertensive disease of small coronary arteries has still to be established.
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PMID:Pathophysiology and clinical aspects of hypertensive hypertrophy. 810 41

Delayed potentials (DP) (ECGHA) are markers of the occurrence of ventricular rhythm disturbances, and have a prognostic value after myocardial infarction. In hypertensive heart disease, the prevalence of DP is variable according to the literature (1-40%) and their prognostic significance is not known. We examine the frequency of DP in hypertension (HT) and the relationship between DP and left ventricular hypertrophy (LVH) as defined by echocardiographic estimation of the LV mass index (LVMI). We investigated 50 consecutive patients with essential HT who were being assessed as regards cause and effects of HT. Exclusion criteria were coronary artery disease, bundle branch block and poor echocardiographic trace. ECGHA was registered by means of ART device. The presence of DP as defined according to the criteria of Kacet. LV mass was determine according to the method of Penn and LVH defined according to the criteria of Devereux. Besides LVMI, were examined age, sex, duration of HT, micro-albuminuria, LVH on ECG (Sokolow index and strain-ECG). There were no correlations between the different variables studied and the presence of DP. The results relating to LVMI are shown in Table. There were no correlation between DP and LVH on echography. Other explanations, electrophysiologic, ischemic and histological may explain the greater incidence of BP observed in hypertensive heart disease. [table: see text] The prevalence of DP was not significantly different as regard the presence or absence of LVH (35% vs 25%; p = 0.53). In the 10 patients with the highest LVMI, the DP were enregistered 3 times.
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PMID:[Delayed potentials and left ventricular hypertrophy]. 812 12

The main important diagnostic and therapeutic problems in hypertensive heart disease refer to the further improvement in the diagnostic procedures in hypertensive hypertrophy; moreover, structural changes of the hypertrophied myocardium have to be analyzed. Quantitative findings concerning the coronary circulation as well as the global and regional myocardial perfusion are desirable. The incidence of ventricular arrhythmias has to be clarified. Further diagnostic studies are needed with regard to the rheological changes as well to the mechanisms for silent and manifest myocardial ischemia. From the therapeutic point of view future studies are desirable concerning the regression of myocardial and vascular hypertrophy, with the aim to find out the optimal therapy for treating both high blood pressure and the hypertension induced structural myocardial and vascular alterations.
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PMID:[Diagnostic and therapeutic problems in hypertensive heart disease]. 814 58

Left ventricular topography and diastolic and systolic functions were studied in 41 patients with essential hypertension (group 1) and 33 age-matched normal adults (group 2) by Doppler echocardiography. In group 1 54% had LV concentric hypertrophy, 19% had combined concentric hypertrophy and eccentric remodeling, and 27% had concentric remodeling. LV systolic function was within the normal range. In concentric LV remodeling, the EDV was significantly decreased (compared with group 2) (84 +/- 15 vs 130 +/- 38 ml, p < 0.05), whereas the NPFR was normal (2.89 +/- 0.65 vs 3.22 +/- 0.83 sec-1, p = NS). In concentric hypertrophy, LV end-diastolic and end-systolic volumes were normal, but the NPFR was decreased (2.04 +/- 0.59 sec-1). Patients with concentric hypertrophy and eccentric remodeling had the largest end-diastolic (140 +/- 48 ml) and end-systolic (62 +/- 32 ml) volumes and the lowest NPFR (1.67 +/- 0.69 sec-1). The LVMI inversely correlated with the NPFR (r = -0.89, p < 0.0001). Thus LV concentric hypertrophy with or without concentric or eccentric remodeling is seen in patients with systemic hypertension. A decrease in peak filling occurs early in the evolution of hypertensive heart disease and is observed even when systolic performance is still normal.
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PMID:Doppler echocardiographic evaluation of the spectrum of left ventricular diastolic dysfunction in essential hypertension. 815 30


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