Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Consecutive hypertensives admitted with cardiovascular complications were studied. One hundred and eight complicated hypertensives (10%) out of 1,066 medical admissions were seen in the three month study. Thirty three per cent had cerebrovascular disease, 30% ischaemic heart disease, 2% had malignant hypertension and 85% had hypertensive heart disease. All patients had uncontrolled hypertension at admission (mean blood pressure 184/115 mmHg). Twenty-four patients (22%) were newly diagnosed; of the rest of previously diagnosed hypertensives (78%), 3% had never been on treatment and 56% had dropped out of treatment, which explained their ineffective blood pressure control. However, 18% of patients had apparently been on regular follow up and treatment, and yet their blood pressure control was poor. Many patients had evidence of renal disease. The prevalence of cardiovascular risk factors was also high; 56% had hypercholesterolaemia; 46% had hypertriglyceridaemia; 44% smoked, 38% were overweight or obese, and 18% were diabetic. This indicates that hypertension is best regarded as an ingredient of a cardiovascular risk profile and its management requires multifactorial correction of all risk factors identified.
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PMID:The Mentakab Hypertension Study project. Part I--Complicated hypertensives in hospital: who are they? 177 3

An impaired coronary vasodilator reserve has been demonstrated in all stages of hypertensive heart disease but is most likely in the setting of hypertrophy. The decrease in coronary flow reserve has, however, not been predictable previously. We postulated that flow reserve depression might be related to a left ventricular mass threshold. Seventy-two patients (82% with hypertension) with suspected ischemic heart disease who were found to be free of significant coronary artery disease at cardiac catheterization were evaluated utilizing the intracoronary Doppler catheter and two-dimensional directed M-mode echocardiography for determination of coronary flow reserve and left ventricular mass. For left ventricular mass indexed (LVMI) by body surface area (BSA) greater than or equal to 50% above normal using established gender-specific norms, American Society of Echocardiography (ASE) and PENN methods (correction of LV mass by regression equation agreeing with necropsy estimates of mass) predicted impairment of flow reserve (p = 0.005 and 0.009, respectively). Unindexed left ventricular mass and LVMI by height were not helpful in this regard. Using the ASE method for LV mass determination, coronary flow reserve was moderately depressed (2.4 +/- 1.0) for those with LVMI greater than or equal to 50% above normal; in comparison, flow reserve was normal (3.5 +/- 1.3) for those with LVMI less than 50% above normal. A rare patient was able to maintain a normal flow reserve when ASE- and Penn-indexed mass estimates were greater than or equal to 50% above normal, but only in the setting of a markedly elevated mean arterial pressure.
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PMID:Relationship of left ventricular mass to impairment of coronary vasodilator reserve in hypertensive heart disease. 182 83

Hypertensive heart disease is a frequent complication in hypertensive African-Americans because of inadequate high blood pressure control. Moreover, African-Americans may be predisposed to develop LVH earlier in life and more readily than Caucasians, and it may be more malignant. The appearance of both LVH and congestive heart failure are ominous developments in individual patients, and early detection of LVH is mandatory for adequate management and reversal of this complication, if possible. Additional research is needed, and new, sensitive tools for detecting LVH will accelerate such studies. Further investigations are also needed on the reversibility of LVH, preferred antihypertensive agents for accomplishing reversal, and whether expected benefits result.
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PMID:Hypertensive heart disease in African-Americans. 182 78

Cardiac remodeling constitutes a risk factor in cardiovascular disease. It may occur in a variety of circumstances. In hypertension and following myocardial infarction, pharmacological intervention in the remodeling process has been the subject of several studies. But the mechanisms of action of drugs that do contribute to regression of the remodeling response are still a matter of debate. Much of the confusion around the subject comes from the fact that classic arteriolar vasodilators do not result in such regression in hypertensive cardiac hypertrophy. This paper reviews some of the literature to examine whether there is indeed an exceptional position for vasodilators in hypertensive heart disease. Although, conceptually, arteriolar dilatation, and thus afterload reduction, might also have favorable effects on the remodeling response following myocardial infarction, clinical studies suggest the opposite. In the present paper, possible mechanisms are discussed, and evidence is presented that shows that hydralazine has an unexpected effect on the remodeling response at the level of the extracellular matrix.
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PMID:Cardiac remodeling in hypertension and following myocardial infarction: effects of arteriolar vasodilators. 182 79

In arterial hypertension, casual blood pressure seems to be weakly related to the level of cardiac involvement. The aim of the present study was to assess if blood pressure during ambulatory monitoring, and during different stress tests, is a stronger predictor of anatomical and functional changes observed in hypertensive heart disease. To this aim, 29 untreated patients with borderline-to-moderate essential hypertension underwent an echo-Doppler evaluation to determine left ventricular thickness and mass. From transmitral flow, the ratio between late and early filling velocities (A/E ratio) was used to assess left ventricular diastolic behaviour. On the same day that ultrasonic study was carried out, we also measured a set of casual blood pressures; conducted a mental arithmetic test (standardized series of mental subtractions); a handgrip test (30% of maximum voluntary contraction for 3 minutes); and performed noninvasive ambulatory monitoring of blood pressure (Spacelabs 5200). Significant relationships were observed between left ventricular mass and both night-time systolic blood pressure (r = 0.46, P less than 0.02) and peak systolic blood pressure during mental stress (r = 0.39, P less than 0.05). The A/E ratio was significantly associated with casual systolic and diastolic blood pressure (r = 0.45, P less than 0.02; r = 0.38, P less than 0.05, respectively); day-time diastolic blood pressure (r = 0.47, P less than 0.02); night-time systolic and diastolic blood pressure (r = 0.44, P less than 0.05; r = 0.42, P less than 0.05 respectively); and peak systolic blood pressure during the mental arithmetic test (r = 0.44, P less than 0.05). Our results seem to confirm the presence of a relationship between causal blood pressure and left ventricular filling. Moreover, the transmitral flow seems to be dependent on both mean levels of blood pressure on ambulatory monitoring and systolic blood pressure during mental stress. As concerns left ventricular mass, the correlations observed support the weakness of the links between blood pressure and left ventricular anatomy.
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PMID:Casual, ambulatory and stress blood pressure: relationships with left ventricular mass and filling. 183 35

The cardiac organ manifestation of arterial hypertension comprises the myocardium itself with left-ventricular hypertrophy, the interstitium with perivascular and interstitial fibrosis, and the coronary circulation with disease of large and small coronary arteries. The consequences of the sum and interactions of these cardiac organ manifestations have an impact on left-ventricular systolic and diastolic function, the ischemic risk, and the occurrence of arrhythmias in hypertensive patients. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive coronary microangiopathy in order to improve the coronary reserve and to reduce the ischemic risk. Regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympatholytic substances). While normal systolic function was maintained in the compensated stage of hypertensive hypertrophy and was not significantly influenced by antihypertensive therapy, diastolic function was impaired in a very early stage of arterial hypertension. Both the phase of isovolumic relaxation and the phase of early diastolic filling were imparied, while after long-term antihypertensive treatment with Ca-channel blockers of the dihydropyridine type or ACE inhibitors, only the latter one was improved. From preliminary results there is clinical evidence that hypertensive disease of small coronary arteries can be reversed after long-term antihypertensive treatment with a consequently improved coronary reserve and a reduced ischemic risk. Moreover, to what extent the prognosis of hypertensive heart disease can be improved by reversal of myocardial hypertrophy and disease of small coronary arteries is yet unknown.
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PMID:Long-term treatment in arterial hypertension for protecting hypertrophic myocardium. 183 50

Differentiation between hypertrophic cardiomyopathy and hypertensive heart disease is a diagnostic challenge. M-mode echocardiography only permits assessment of hypertrophy in limited areas of the left ventricular wall. 2-D echocardiography allows visualization of most of the myocardium. To assess the reliability of conventional M-mode echocardiographic and 2-D echocardiographic criteria in patients with hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HY), 30 patients with hypertrophic cardiomyopathy and 30 patients with hypertension and severe cardiac hypertrophy were examined using M-mode and 2-D echocardiography. Although the M-mode echocardiographic features showed statistically significant differences between the mean values in the two groups, the degree of overlap made the differentiation of the individual patients difficult. The diagnostic sensitivity and specificity of classic echocardiographic features were assessed: ventricular septal thickness greater than or equal to 1.5 cm, 90% and 43% (sensitivity and specificity, respectively); ventricular septal thickness to posterior wall ratio greater than or equal to 1.5, 83% and 56%; cross-sectional area at papillary level greater than 21 cm2m-2, 80% and 73%; septal segment of the myocardial ring at papillary level greater than 6.5 cm2m-2, 80% and 87%; and the combined criteria of cross-sectional area at papillary level greater than 21 cm2m-2 and septal segment greater than 6.5 cm2m-2, 77% and 93%. Quantitative 2-D echocardiography is useful to differentiate patients with hypertrophic cardiomyopathy from those with secondary myocardial hypertrophy due to hypertension. Hypertrophic cardiomyopathy is characterized by a spectrum of different morphological patterns of hypertrophy. Patients with the predominant region of hypertrophy in the anterolateral free wall or the apical region of the left ventricle were not detected with our quantitative method. Patients with this type of hypertrophy are relatively rare in the western population.
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PMID:Morphological quantification and differentiation of left ventricular hypertrophy in hypertrophic cardiomyopathy and hypertensive heart disease. A two dimensional echocardiographic study. 213 78

In selected patients with systemic hypertension it may be difficult to ascertain whether left ventricular (LV) hypertrophy is a secondary end-organ consequence of long-term elevations in blood pressure or, alternatively, a manifestation of a coexistent primary hypertrophic cardiomyopathy. To address this issue and better characterize LV hypertrophy in systemic hypertension, 2-dimensional echocardiography was used to define the patterns of LV hypertrophy in 102 patients with sustained systemic hypertension and marked degrees of wall thickening. Patients ranged in age from 31 to 88 years (mean 61) and were predominantly female (58%); all were black. By selection, each patient had a maximal LV wall thickness of greater than 15 mm (range 16 to 29). Distribution of hypertrophy was judged to be symmetric (i.e., concentric) in most patients (67 of 102, 66%). However, a substantial proportion (35 patients, 34%) demonstrated nonuniform, asymmetric patterns of hypertrophy in which at least 1 segment of the LV wall was at least 1.5 times the thickness of any other. In these 35 patients, the distribution of hypertrophy was similar to that characteristic of the morphologic spectrum of hypertrophic cardiomyopathy, with thickening of portions of both the ventricular septum and free wall in 16 patients, anterior and posterior ventricular septum alone in 11 patients and segmental involvement of only the anterior ventricular septum in 8. Patients with asymmetric patterns of wall thickening did not differ from the patients with symmetric hypertrophy with regard to age, sex or clinical findings. Asymmetric LV hypertrophy appears to represent an important feature of the morphologic spectrum of severe hypertensive heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diversity of patterns of hypertrophy in patients with systemic hypertension and marked left ventricular wall thickening. 213 47

Coronary hemodynamics (coronary blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical essential hypertension. Significant reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Extracoronary reasons for these phenomena were ruled out. Considerable thickening of the coronary resistance vessels (medial hypertrophy) in hypertensive hypertrophy associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impairment of coronary flow. After long-term pharmacotherapy there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible approach to the rational prevention of cardiac failure in hypertensive patients. For future investigations, controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.
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PMID:Significance of coronary circulation in hypertensive heart disease for development and prevention of heart failure. 213 55

Hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. Because the prognosis of arterial hypertension is determined to a considerable extent by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive heart failure. A further goal of therapy is reversal of the hypertensive small coronary disease in order to improve the coronary reserve. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics and angiotensin-converting enzyme inhibitors apply. Whereas the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, angiotensin-converting enzyme inhibitors and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of the hypertensive disease of small coronary arteries has yet to be provided. Moreover, to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy is still unknown.
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PMID:Differential therapy of hypertensive heart disease. 213 59


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