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)

Up to now only 30 to 40% of patients who die suddenly can be identified as likely candidates before the event. Risk factors in these asymptomatic subjects include a familial history of coronary artery disease, high blood cholesterol levels, hypertension, smoking and, more importantly, an abnormal ECG at rest or during exercise. The predictive value of these abnormalities is too low to justify more detailed clinical investigations in most of these asymptomatic subjects. Exceptions might be the group of patients with multiple risk factors and competitive sportsmen. Sudden cardiac death is a well known complication in patients with hypertrophic and dilated cardiomyopathy. Risk factors in hypertrophic cardiomyopathy include a familial history of this disease, syncope and increasing age. Furthermore, in the adult, the presence of nonsustained episodes of ventricular tachycardia during Holter monitoring seems to indicate an increased risk of sudden cardiac death. In idiopathic dilated cardiomyopathy, the presence of frequent episodes of ventricular pairs and/or episodes of ventricular tachycardia during Holter monitoring, together with a reduced left ventricular ejection fraction, characterises the patient at risk of sudden cardiac death. In patients with coronary artery disease, the patient at risk of sudden cardiac death can be identified by investigating the following: coronary anatomy; global and regional left ventricular function; the presence of ischaemia during rest and/or exercise; the presence of late potentials, by means of the signal-averaged ECG; the presence of spontaneous ventricular arrhythmias (especially sustained and nonsustained ventricular tachycardia); and the results of electrophysiological testing. On the basis of these investigations, 3 subgroups can be distinguished: patients at low risk, medium risk, and high risk of sudden cardiac death.
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PMID:Can we predict sudden cardiac death? 171 71

In order to establish a normalizing method for left ventricular filling indexes, peak filling rate (PFR) and time to peak filling rate (TPFR), derived from resting radionuclide ventriculography using Fourier analysis with third-order harmonics, were analyzed in 45 normal subjects, 40 hypertensive patients, and 29 patients with hypertrophic cardiomyopathy. PFR was significantly negatively correlated with age (r = -0.62) and significantly positively correlated with peak ejection rate (PER) (r = 0.58) in normals. TPFR normalized for heart rate (N-TPFR) was correlated positively with age in normals (r = 0.60) and hypertensives (r = 0.49) but not in patients with hypertrophic cardiomyopathy. N-TPFR was not significantly correlated with systolic parameters. A significant relationship between PFR normalized to PER (PFR/PER) and age was observed in normals (r = -0.58) but not in patients with hypertension or hypertrophic cardiomyopathy. To cancel the ageing effect, individual data of PFR/PER and N-TPFR were expressed as a percentage of the predicted regression value in normal subjects (%PFR/PER and %N-TPFR, respectively). Per cent PFR/PER was significantly lower and %N-TPFR was significantly greater in patients with hypertension and hypertrophic cardiomyopathy compared to normals. When normal limits of these indexes were defined as %PFR/PER greater than 80% and %N-TPFR less than 120%, the sensitivity, specificity and diagnostic accuracy of differentiating normals from patients with hypertension or hypertrophic cardiomyopathy were 41 of 45 (91%), 44 of 68 (65%), and 85 of 113 (75%), respectively. These findings indicate that %PFR/PER and %N-TPFR might be more reasonably normalized parameters for describing diastolic filling and its abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normalized left ventricular filling indexes to detect diastolic dysfunction in hypertension and in hypertrophic cardiomyopathy. 174 69

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
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PMID:Etiology and pathogenesis of thromboembolism. 176 43

Midventricular obstruction is an uncommon finding previously defined by catheterization and angiographic techniques in patients with hypertrophic cardiomyopathy. This study describes the clinical and echocardiographic findings of 10 consecutive patients (mean age 73 years) with severe concentric left ventricular (LV) hypertrophy and the unusual finding of a dynamic systolic obstruction located in the midportion of the left ventricle. All patients were known to have chronic hypertension, and none had a history or family history of hypertrophic cardiomyopathy. In each case, a well-defined, high velocity, turbulent jet was identified by Doppler color flow imaging and subsequently confirmed with conventional Doppler techniques. Septal and posterior wall thickness averaged 1.67 and 1.57 cm, respectively. Mean LV mass index was 199 g/m2 and ejection fraction averaged 78%. Peak systolic velocity obtained by continuous-wave Doppler averaged 2.7 m/s and appeared as either a "late-peaking" or a "spike and dome" configuration. Seven of 10 patients gave a history of syncope or severe presyncope at the time of echocardiographic examination. At a mean follow-up of 1 year, syncope or presyncope had resolved in 5 patients in whom medication was adjusted based on the ultrasound study, but persisted in 2 patients in whom diuretic therapy was continued. It is concluded that obstruction to systolic flow can occur at the mid-LV level in some patients with severe concentric LV hypertrophy and avoidance of medication known to lower LV volume may relieve symptoms of transient inadequate cardiac output.
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PMID:Midventricular obstruction associated with chronic systemic hypertension and severe left ventricular hypertrophy. 183 13

Seven adult patients with old and severe arterial hypertension were found to have hypertrophic cardiomyopathy with left ventricular obstruction demonstrated by an isoproterenol test. Whenever feasible, confirmation that systolic obstruction of the left ventricular outflow tract was due to anterior systolic movement of the mitral valve was obtained. Echocardiography revealed a number of ultrasonic features (asymmetrical septal hypertrophy, small left ventricle and clear-cut reduction of the left ventricular outflow tract) which put these cases closer to the primary hypertrophic cardiopathy group than to the hypertensive cardiomyopathy group, with a similar history of hypertension. Detecting this group is facilitated by the use of vasoactive drugs in patients with these echocardiographic features. This is important since there is a risk of poor tolerance to vasodilators, notably nitrates, which may suddenly reveal the left ventricular dynamic obstruction syndrome. These patients are also exposed to paroxysmal atrial fibrillation.
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PMID:[Hypertrophic cardiomyopathy with left ventricular dynamic obstruction syndrome in hypertensive adult patients]. 183 84

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.
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PMID:[Angina due to microvascular pathology]. 184 63

Withdrawal of beta-blocker therapy has been associated with the development of adrenergic hypersensitivity and adverse clinical effects in patients with coronary artery disease and hypertension. The aim of this study was to establish the occurrence and clinical significance of adrenergic hypersensitivity after abrupt withdrawal of long-term beta blockade in hypertrophic cardiomyopathy. Beta-adrenergic sensitivity was measured using the isoprenaline chronotropic dose25. Symptom assessment chronotropic dose25 calculation, bicycle exercise, echocardiography and Holter monitoring were performed while the patient received beta-blocker therapy and repeated on days 2, 4, 6, 8 (acute withdrawal period) and on day 21 after abrupt withdrawal. The study was terminated after 7 patients had been studied because all patients experienced a marked deterioration in symptoms and several clinical events had occurred. The chronotropic dose25 (mean +/- standard deviation) demonstrated beta 1-adrenergic hypersensitivity with a minimal value of 1.6 +/- 0.8 micrograms during the acute withdrawal period compared with 3.8 +/- 1.7 micrograms on day 21 (p = 0.003). Heart rates during rest and exercise showed an overshoot increase during the acute withdrawal period. The maximal 24-hour ventricular ectopic count was higher during the acute withdrawal period than during day 21 (p = 0.04). Of 3 patients with inducible outflow tract gradients, 2 developed resting gradients greater than 30 mm Hg during the acute withdrawal period. There was an increase in peak late filling velocity of mitral inflow after beta-blocker withdrawal. In conclusion, transient beta-adrenergic hypersensitivity occurs after beta-blocker withdrawal in hypertrophic cardiomyopathy and is associated with significant physiologic changes and adverse clinical consequences.
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PMID:Adrenergic hypersensitivity after beta-blocker withdrawal in hypertrophic cardiomyopathy. 189 84

Clinical implications of diffuse slow washout of thallium-201 (DSWO) in exercise-redistribution myocardial SPECT were studied. Thallium-201 washout rate was calculated by Bull's-eye method. DSWO was defined as having abnormal thallium-201 washout rate (less than 30% per 3 hours) in more than two thirds of each coronary artery (CA) area. OF 974 patients whose exercise heart rate exceeded 120/min, 51 (5.2%) showed DSWO and coronary angiography was performed in 43. Twenty-three patients (53%) showed triple vessel disease (3VD), 8 (19%) showed single or double vessel disease (1VD/2VD) and 12 (28%) showed normal CA. Patients with normal CA consisted of 6 patients with hypertrophic cardiomyopathy (HCM), 5 with hypertension (HT) and one with electrocardiographic abnormality only. The causes of DSWO were assessed from the history of effort angina (EA) and congestive heart failure (CHF), delayed fill-in of the perfusion defect and the ratio of lung to heart thallium-201 activity (L/M) at exercise as an indicator of the left ventricular (LV) function. High prevalence of EA (74%), high incidence of scintigraphic delayed fill-in (83%) and normal L/M suggested diffuse LV ischemia as the cause of DSWO in 3VD. On the other hand in patients with 1VD/2VD, LV dysfunction at exercise was considered as the cause of DSWO because of low prevalence of EA (13%) and scintigraphic delayed fill-in (13%) (p less than 0.01, p less than 0.005 each vs 3VD), and high L/M (p less than 0.001 vs 3VD) and high prevalence of CHF (38%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical implications of diffuse slow washout of thallium-201 in exercise stress myocardial SPECT]. 192 Sep 45

To investigate left atrial (LA) booster pump function in hypertrophic cardiomyopathy (HC), LA and left ventricular pressure-volume loops were estimated in 5 control subjects, 6 patients with essential hypertension and 11 patients with HC. Investigation of LA preload revealed that LA pressure and volume immediately before LA contraction were both increased in patients with hypertension (10 +/- 5 mm Hg, 71 +/- 19 ml/m2) compared with control subjects (7 +/- 1 mm Hg, 59 +/- 6 ml/m2), and even more increased in patients with HC (16 +/- 7 mm Hg, 81 +/- 25 ml/m2). Investigation of LA afterload revealed that the left ventricular chamber stiffness constant was higher in patients with hypertension (0.035 +/- 0.015) than in control subjects (0.028 +/- 0.009), and even more increased in patients with HC (0.056 +/- 0.017). LA stroke work index was higher in patients with hypertension (116 +/- 34 mm Hg.ml) and HC (115 +/- 19 mm Hg.ml) than in control subjects (87 +/- 23 mm Hg.ml). Investigation of LA ejection revealed that LA stroke index was higher in patients with hypertension (24 +/- 5 ml/m2) than in control subjects (18 +/- 4 ml/m2) and patients with HC (18 +/- 2 ml/m2), and LA ejection fraction was lower in patients with HC (23 +/- 6%) than in control subjects (32 +/- 7%) and patients with hypertension (34 +/- 8%). In patients with HC, LA function curve showed a shift to the lower right, and LA stroke index was inversely correlated (r = -0.76) with LA afterload. This study suggests that LA booster pump failure due to LA afterload mismatch exists in HC.
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PMID:Left atrial afterload mismatch in hypertrophic cardiomyopathy. 192 18

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


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