Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, independent contribution of age, HR, BMI, casual and ambulatory blood pressure, LVM and LVEF in evaluating diastolic filling have been investigated in 34 never-treated hypertensive patients and in 15 healthy normotensive subjects. All the subjects were free from coronary artery disease, valvular disease, heart failure, renal disease and psychiatric problems. All the hypertensive subjects (never treated) were subgrouped according to presence or absence of LVH. The PFR decreased significantly and tPFR increased significantly in hypertensive patients in comparison with normotensive subjects and they did not change in the presence vs absence of LVH. The PFR was inversely correlated with BMI, age, 24-h mean SBP and with 24-h DBP. In multiple regression analysis, PFR decreased with BMI, age, 24-h mean SBP and DBP but not with LVMI. These results suggest that BMI, age and 24-h mean blood pressure were the major determinants of PFR abnormalities in hypertensive patients.
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PMID:Rapid left ventricular filling in untreated hypertensive subjects with or without left ventricular hypertrophy. 142 72

48 patients with chest pain or unexplained heart failure were examined with exercise test, systolic time intervals, apexcardiogram and left- and right-sided heart catheterization including coronary arteriography. The 23 patients with ischemic heart disease (IHD) and 19 patients with congestive cardiomyopathy (COCM) could as groups be separated by several of the parameters. Two major patterns of change were present when using the whole range of parameters, probably reflecting that the heart and circulation had compensated for left ventricular dysfunction in different ways in IHD and COCM. Comparing patients with the same ejection fraction (EF), preejection-period index (PEPI) pre-ejection-period/left ventricular ejection time (PEP/LVET) and systolic blood pressure/left ventricular end systolic volume index (SBP/LVESVI), were all more abnormal in patients with COCM than with IHD at most EF levels. The best separation between the diseases was obtained using exercise capacity in combination with PEP/LVET. The correlations between invasive and noninvasive parameters underlined that no single parameter can satisfactorily characterize the circulatory function in patients with individual differences in preload, afterload, pulse rate, cardiac volumes, compliance and contractility. No or poor correlations were found between exercise capacity and the different function parameters used.
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PMID:Different patterns of hemodynamic abnormalities in patients with ischemic heart disease compared with patients with congestive cardiomyopathy. 371 97

Studies of cardiac performance in hypertension have often been restricted to cardiac output determinations, although the latter alone are inadequate for that purpose. To define the range of cardiac performance in hypertension, the response of left ventricular filling pressure to increased workload (static exercise) was determined in 39 subjects--eight normotensive (NT) volunteers, seven patients with borderline hypertension (BLH), and 24 essential hypertensives (EH), of age-matched groups. A rise of mean pulmonary wedge pressure (PWP) by 5 mm Hg or more during maximum handgrip (HG) was considered "abnormal" for a workload (SBP x HR x 10(-3)) increase of greater than or equal to 25%. All NT subjects and all patients with BLH as well as 16 of the 24 EH (EH-I) showed normal cardiac performance by this definition. In contrast, PWP increased greater than or equal to 5 mm Hg during HG in eight patients with EH (EH-II). The calculated increase in cardiac workload was not significantly different among the four groups (+5, 5.8, 5.4 and 5.5 respectively). Beta blockade (propranolol, 10 mg i.v.) slowed heart rate in all subjects and reduced SBP x HR product in all groups both at rest and during HG. Responses of PWP to HG were widely divergent in the different patients. However, as a group those patients with "impaired cardiac performance" before propranolol (EH-II) had a greater reduction in performance following propranolol than EH-I or NT. This study suggests that adrenergic support of cardiac performance might be important in some hypertensive patients with no evidence of heart failure.
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PMID:Sympathetic contribution to the cardiac response to stress in hypertension. 684 61

Thalassaemia major determines an impaired effort tolerance because of a condition of severe anaemia, progressive left ventricular dysfunction, pulmonary circulation compromise. The aim of our study is to evaluate haemodynamic response to exercise in thalassaemic patients without clinical features of heart failure. We have selected 13 patients affected by thalassaemia major (Thal+; 10-18 years). Each patient was transfused when haemoglobin values were < 9-9.5 g/dl and was treated with desferrioxamine (40 mg/kg sc) when serum ferritin values were > 2,000 ng/ml. Thal+ patients were compared with normal subjects (Thal- 10-16 years). No patient assumed hypotensive therapy, no had familiar history of hypertension. Both groups have undergone an ergometric stress test at the cycloergometer, with increase of 25 W every 2 min, up to the reaching of the maximum age-related heart rate, or up to muscle exhaustion or unbearable dyspnea, followed by a 10 min recovery phase. The following parameters were taken in consideration: systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), the product of the heart rate by the systolic blood pressure (DP), at rest, at the maximum common work (MCW), at maximum stress and in the recovery phases. At rest, only DP showed significant differences between the two groups: in Thal+ patients higher than in Thal- (p = 0.045). At the MCW, Thal+ patients had SBP (p = 0.019), DBP (p = 0.01), HR (p = 0.035) and DP (p = 0.003) higher than Thal- patients. At maximum stress only DBP showed significant differences in Thal+ patients (p = 0.019), although Thal+ patients achieved lower levels of workload (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiovascular adaptation to the stress test in subjects with Cooley's disease]. 780 70

1. Intravenous ACE inhibitor therapy appears to have a role in the treatment of acute heart failure and early after myocardial infarction. Practical experience with intravenous administration with activation of renin is limited. We report responses to perindoprilat (Pt, 0.67 mg) or placebo (P) infused over 4 h in normotensive male volunteers (n = 12, 19-28 years, 53-77 kg) with double-blind, placebo controlled salt depletion (SD) or salt repletion (SR) as a model of the activated renin system. 2. Salt depletion caused no significant fall in serum sodium (P, 139.4 +/- 2.4; Pt, 138.3 +/- 1.9) compared with salt replete preparation (P, 139.9 +/- 1.2; Pt, 139.7 +/- 0.9) but elevation of plasma renin activity 2-3-fold. Pretreatment baseline systolic blood pressure following salt depletion (P, 121 +/- 9.3/71 +/- 7.9; Pt, 121.5 +/- 9.6/69 +/- 8.1) was higher than following salt replete preparation (P, 114 +/- 9.5/61 +/- 7.2; Pt, 116.9 +/- 6.9/67 +/- 7.2). 3. Baseline corrected supine SBP fell significantly and to a similar extent following active treatment regardless of activation of the renin system (SD, -14.6 +/- 9.5/-9.4 +/- 6.4; SR, -12 +/- 14/-10.1 +/- 6.6) compared with placebo (SD, -6.1 +/- 6/-3.7 +/- 5.6; SR, -4.7 +/- 10/-1.3 +/- 6.5). Heart rate was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses to low dose intravenous perindoprilat infusion in salt deplete/salt replete normotensive volunteers. 783 22

To evaluate the cardiac dysfunction of the cerebral infarction (cerebral thrombosis) patients in the chronic period, non-invasive studies were performed on 45 cerebral infarction patients (CI group: 25 males and 16 females, mean age 64.1 y). Forty hospitalized patient without cerebral infarction served as controls (non-CI group: 23 males and 19 females, mean age 64.8 y). The CI and non-CI group were divided into two sub-groups: patients with a past history of hypertension (HT) and without (NT). In each sub-group, the cardiac functions were compared between CI and non-CI by M-mode and Doppler echocardiography. In echocardiography, research based on the premise that the function of the left ventricle can be divided into preload (EDVi), afterload (SVR), contractility (EF, mVcf, SBP/ESV) and distensibility (E/A). On results show that there were no significant differences in preload, afterload and contractility of the left ventricle between CI and non-CI group in each HT and NT sub group. However, a significant difference was demonstrated in the diastolic function the left ventricle between the two groups in the HT (p = 0.007) and NT (p = 0.04) sub-groups. In conclusion, left ventricle diastolic function was deteriorated in cerebral infarction patients although systolic function not deteriorated. Because diastolic dysfunction may be caused by existing latent heart failure and/or silent myocardial ischemia, echocardiographic study is useful for early detection of left ventricle impairments in cerebral infarction patients.
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PMID:[Study of left ventricular function in cerebral thrombosis with pulsed Doppler echocardiography]. 811 52

A crucial element for weaning patients from cardiopulmonary bypass (CPB) rests on the selection of an appropriate therapeutic regimen. Amrinone, a phosphodiesterase III inhibitor, combines inotropic support with pulmonary and systemic vasodilatation, without increasing heart rate (HR) or myocardial oxygen consumption. These characteristics should be useful in the failing heart during weaning from CPB. Nineteen patients were included in this prospective, open-labelled, phase IV study when systolic blood pressure (DPAP) > 15 mmHg or central venous pressure (CVP) > 15 mmHg, during progressive separation from CPB. At that moment, CPB flow was increased to alleviate heart failure and amrinone administered as a bolus (0.75 mg.kg-1) followed by an infusion (10 micrograms.kg-1.min-1). Weaning from CPB was then resumed and haemodynamic variables (SBP, DPAP, CVP and HR) were compared with those measured at CPB flow when failure had first occurred. Failure to wean from CPB occurred at 57 +/- 28% of full pump flow. After the amrinone bolus, DPAP and CVP decreased by 20% and 21% respectively. Subsequently, 16 patients required the infusion of norepinephrine (4-8 micrograms.min-1) to maintain a SBP > 80 mmHg. Heart rate remained unchanged after the bolus of amrinone, after separation from CPB, and no arrhythmias were noted. Successful weaning from CPB was possible 12 +/- 8 min after the amrinone bolus. Weaning resulted in a cardiac index similar to that measured pre-bypass. Amrinone is rapidly effective during weaning from CPB and, in combination with norepinephrine, provides the necessary inotropic support during this unstable period.
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PMID:Amrinone, in combination with norepinephrine, is an effective first-line drug for difficult separation from cardiopulmonary bypass. 840 12

1. Physical training has been proposed to increase vagal control of heart rate in chronic heart failure. We studied the effects of physical training on cardiovascular control in 6 moderate to severe heart failure (NYHA II-III) patients and 6 age matched normal controls in a randomized controlled cross over trial (Training vs Detraining). 2. Five weeks training (20 min/day, 5 days/week bicycle exercise) increased peak VO2 in both C (from 31.2 +/- 1.4 to 37.7 +/- 2.4 ml/kg/min p < 0.01) and CHF patients (from 12.16 +/- 2.2 to 14.13 +/- 2 ml/kg/min p < 0.05). The sympathovagal control of heart rate and sympathetic control of the resistance vessels was assessed by the power of the oscillations (LF:0.03-0.15 Hz index of sympathetic activity, HF: 0.18-0.35 Hz index of vagal activity) in RR interval, blood pressure (systolic and diastolic by Finapres) and respiration by autoregressive spectral analysis, during free and controlled breathing (15b/min), in order to increase vagal activity. 3. T increased heart rate vagal control both in C (LF/HF ratio fb to cb: (D) 1.73 +/- 0.35 to 1.19 +/- 0.43 p = NS: (T) 2.9 +/- 1.2 to 1.13 +/- 0.3 p < 0.05) and in CHF patients (LF/HF ratio fb to cb: (D) 2.05 +/- 0.56 to 1.24 +/- 0.21 p = NS; (T) 2.6 +/- 0.89 to 0.87 +/- 0.15 p < 0.05; and in cb HF%: 36.2 +/- 2.7 (D) to 46.2 +/- 4.8 (T) p < 0.05). Before T, the sympathetic modulation of peripheral vessels (% LF compared to total variability) was depressed in CHF vs C (SBP: 9 +/- 2 vs 42 +/- 12% p < 0.05; DBP: 29 +/- 7 vs 55 +/- 31%, p < 0.05), and increased significantly after T in CHF (SBP from 9 +/- 2 (D) to 19 +/- 5% (T) p < 0.05; DBP from 29 +/- 7 to 41 +/- 11% (T) p < 0.05). This suggests an overall increase of autonomic control, both vagal on the heart and sympathetic on the peripheral vessels, in CHF by physical training.
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PMID:Physical training enhances sympathetic and parasympathetic control of heart rate and peripheral vessels in chronic heart failure. 881 40

Calcium antagonists have antihypertensive and antianginal properties. In heart failure, however, their use can be hazardous, as systolic function can deteriorate. This may not be true of the new calcium antagonist mibefradil, which has a new chemical structure. Calcium antagonists may also be beneficial for diastolic left ventricular function in coronary artery disease. To investigate the possible effects of mibefradil on diastolic left ventricular function, we performed the present study as a multicenter, double-blind,placebo-controlled, multiple-dose safety trial. Fifteen patients with New York Heart Association (NYHA) class II or III for dyspnea and depressed ejection fraction (<40%) due to a previous myocardial infarction were investigated. The measured nuclear angiographic parameters included ejection fraction (EF), peak ejection rate (PER), and peak filling rate (PFR). Systolic and diastolic blood pressure (SBP, DBP) and heart rate (HR) were also obtained. Group I (5 patients) received placebo medication; group IIA (6 patients) received mibefradil 6.25, 12.5, or 25 mg/day; and group IIB (4 patients) received mibefradil 50 or 100 mg/day. Measurements were made before and after the first dose and after 1 week of treatment before and after the final dose. Mibefradil clearly decreased HR (repeated-measures analysis of variance p < 0.05). No statistically significant effects of mibefradil were noted on SBP or DBP or on systolic and diastolic left ventricular function. In our study conditions, mibefradil caused no worsening of systolic function and preserved diastolic function in short-term treatment of patients with decreased EF and heart failure.
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PMID:Effect of mibefradil on left ventricular diastolic function in patients with congestive heart failure. 885 34

Left ventricular hypertrophy is associated with an increased cardiovascular mortality in hypertension. A potential role of ventricular arrhythmias is debated but not yet determined. The purpose of this study was to evaluate whether the presence of arrhythmias would ascribe any additional risk to cardiovascular mortality beyond that related to the presence of left ventricular hypertrophy. From November 1988 to February 1991, 40 mild to severe hypertensive patients (mean SBP, DBP 183/117 mm Hg) were submitted to clinical, echocardiographic and electrocardiographic evaluations complemented by 24-h Holter monitoring and then followed until November 1996. The Kaplan-Meier method supplemented by the Cox multiple regression model were performed to identify the variable(s) associated with fatal cardiovascular outcome. Twelve cardiovascular fatalities occurred as a consequence of sudden death (n = 4), stroke (n = 4), heart failure (n = 2) and myocardial infarction (n = 2). In comparison with patients who survived, those dying from cardiovascular causes had a greater percentage of electrocardiographic left ventricular hypertrophy (83 vs 36%, P = 0. 0037) and couplets of ventricular ectopic beats (58 vs 18%, P = 0. 0467). In addition, they showed larger left ventricular diastolic diameter (60 +/- 10 vs 53 +/- 8 mm), mass index (248 +/- 67 vs 154 +/- 57 g/m2) and posterior wall thickness (12 +/- 2 vs 10 +/- 2 mm), as well as shorter left ventricular fractional shortening (0.23 +/- 0.8 vs 0.32 +/- 0.9). Univariate analysis showed that electrocardiographic left ventricular hypertrophy and strain, mass index, end-systolic wall stress, fractional shortening and the presence of couplets were significantly related to cardiovascular mortality. However, only mass index was shown to be independently associated with cardiovascular death. In conclusion, left ventricular hypertrophy predicts cardiovascular outcome, regardless of the presence of other signs of cardiac damage, including ventricular arrhythmia.
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PMID:Left ventricular hypertrophy predicts outcome of hypertension regardless of the type of ventricular arrhythmia present. 1048 71


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