Left ventricular adaptation to hypertension and plasma renin activity

Chronic pressure and volume overload result in morphologically and functionally distinct forms of myocardial hypertrophy. In essential hypertension, the respective effect of these factors on the morphology of the left ventricle remains unknown. In the present study, we hypothesised that activity of the renin angiotensin system (assessed by plasma renin activity) may be associated to the variability of the left ventricular adaptation to essential hypertension. To assess this relation, we categorised by echocardiography 333 never-treated hypertensive patients, according to values of left ventricular mass and relative wall thickness. Higher systolic and pulse arterial pressure was strongly associated with concentric left ventricular hypertrophy (27% of hypertensives). When compared to the normal left ventricle group, patients with eccentric left ventricular hypertrophy (15% of hypertensives) had a high cardiac index (5 +/- 1 vs 4 +/- 0.8 L/min/m2; P = 0.0001), a lower basal plasma renin activity (0.81 +/- 0.63 vs 1.45 +/- 1.3 ng/ml/h; P = 0.02) and similar mean values of left ventricular performance and glomerular filtration rate. A tendency for depressed myocardial contractility assessed by the midwall shortening/end-systolic stress was associated with concentric left ventricular remodelling and hypertrophy when compared to hypertensive with a normal left ventricle. In conclusion, at the early phase of essential hypertension, in patients without renal dysfunction, each anatomic pattern of cardiac adaptation to hypertension was associated with a distinct profile of haemodynamics, myocardial function and activity of the renin-angiotensin system. Journal of Human Hypertension (2000) 14, 181-188.     

Creatine kinase activity and temperature in children after cardiac surgery

The preoperative and postoperative serum creatine kinase (CK) activity and postoperative temperatures were studied in children undergoing surgery for congenital heart disease. Using multiple linear and logistic regression and analysis of variance, associations were found between postoperative CK activity (>2,000 IU/L) and the use of succinylcholine, aortic cross-clamp time (>30 minutes), cardiopulmonary bypass time (>60 minutes), the development of fever (>38.5°C), and complications. Complications were defined as hemodynamic instability, poor peripheral perfusion, metabolic acidosis, and eventual multiple organ failure. Associations were also found between postoperative fever and the development of complications. The results suggest that children who develop serum CK elevations greater than 2,000 IU/L and fever greater than 39.5°C during the early postoperative period after cardiac surgery more often develop serious complications.     

Relationship between renin activity and aldosterone release in the patients with low cardiac output syndrome after open cardiac surgery.

Plasma renin activity and aldosterone concentration were measured by radioimmunoassay technique in seven patients with low cardiac output syndrome after open cardiac surgery. Plasma renin activity and aldosterone concentration markedly increased, and plasma renin activity was well correlated with plasma aldosterone concentration. Plasma renin activity and aldosterone concentration, however, had no direct correlation with plasma sodium and potassium concentration or administered doses of inotropic agent, potassium and diuretic. Sodium and potassium balance was closely correlated with plasma aldosterone concentration. In the present study, it was suggested that the secondary hyperaldosteronism following low cardiac output syndrome after open cardiac surgery was mainly induced by the increased release of renin and that it influenced on the balance of sodium and potassium metabolism under such disturbed circulatory circumstances.     

Normal plasma renin activity in low renin hypertension.

Plasma renin activity (PRA) was measured every 4 h during a 24-h period of continuous recumbency in 10 patients with essential hypertension. All had maximum values at 12 midnight, 4 AM or 8 AM. Analysis of our date and that of others indicates that in some patients with "low renin" hypertension (LRH) these noctural peaks are of normal magnitude, occasionally exceeding values obtained after four hours of erect posture. Sleep-induced renin release in these patients is not suppressed despite blunted responses to other stimuli. This suggests that the ability to synthesize and release renin may be normal in these patients. Such peaks were not obserived in all LRH subjects, however. The area enclosed by the recumbent PRA curve was also normal in some, but not all patients with LRH. Low renin hypertension may not be a homogeneous disorder.     

Right ventricular failure after cardiac surgery

Right ventricular (RV) failure remains a major problem in cardiac surgery, particularly in the setting of heart transplantation and following institution of left ventricular support. Experimental studies have shown that RV function is derived from 2 sources: the free wall of the RV and the interventricular septum. Management of RV failure involves not only decreasing RV afterload, but also optimizing both contributions to RV function, which is best achieved by optimizing developed systemic pressure. Techniques for managing the pulmonary circulation and strategies for optimizing RV function in various clinical settings are presented.     

Subpulmonary pleural effusions in children after cardiac surgery.

Postoperative chest radiographs on 100 children who had undergone cardiac operations were evaluated to determine the frequency of subpulmonary effusions after surgery. Of the 83 patients in whom adequate erect postoperative radiographs were available, 9 (11%) had effusions confirmed by lateral decubitus radiographs. On the frontal chest x ray film, the evidence of an effusion was an increase in distance between the diaphragm and air in the gastric fundus, or an apparent elevation of the right hemidiaphragm. None of the patients examined echocardiographically had associated pericardial effusions. When a subpulmonary effusion was detected diuretic treatment was started or continued. None of the patients had radiographic evidence of residual fluid when they were seen two weeks after their discharge from hospital.     

Furosemide and plasma renin activity in essential hypertension.

Changes in arterial blood pressure, renal electrolyte excretion, and plasma renin activity in response to repeated doses of furosemide were measured in 12 patients with essential hypertension admitted to the medical service for electrolyte balance studies. Eighty and 120 mg/day furosemide in divided doses for 5 to 10 days produced a prompt increase in renal sodium excretion. Urinary Na/K concentration ratios, which were elevated during peak natriuresis, returned to control levels following the initial diuretic response. In 2 patients with high initial levels of plasma renin activity, arterial blood pressure was not reduced by furosemide, and more potent antihypertensive agents were required to control the blood pressure. In the remaining patients, furosemide produced a significant decrease in systolic and diastolic blood pressure. There was a general upward shift of plasma renin levels in terms of 24-hour renal sodium excretion in those who demonstrated an antihypertensive response to the drug. However, the average increase in plasma renin activity after repeated doses of furosemide was not statistically significant and no correlation was demonstrated between the level of plasma renin activity after furosemide and the blood pressure lowering effect of the drug.     

Methodologic problems in plasma renin activity measurements.

The influence of pH and angiotensinase inhibitors on the in vitro generation of angiotensin I during PRA measurements has been investigated. PRA values obtained at pH 5.7 are higher than those obtained at pH 7.4. At pH 5.7, values obtained using diisopropylfluorophosphate (DRP 9 mM) as an angiotensinase inhibitor are higher than values obtained with a mixture of dimercaprol (BAL, 1.6 mM) and hydroxyquinoline (8-OHQ, 3 to 4 mM). Since the two methods for inhibiting angiotensinase are completely and equally efficient, it is suggested that these inhibitors might interfere with the renin angiotensinogen reaction. Significant correlations are observed between the PRA values obtained by the different methods which have been studied. Using an incubation pH of 5.7, and BAL and 8-OH quinoline as angiotensinase inhibitors, the distribution of PRA values in a population of 124 hospitalized hypertensive patients ingesting a normal sodium diet had been studied, and it has been demonstrated that the sensitivity of this method of measurement can detect small changes in PRA in patients with low renin activity.     

New-onset sustained ventricular tachycardia after cardiac surgery

BACKGROUND: The de novo occurrence of sustained ventricular tachycardia (VT) after CABG has been described, but the incidence, mortality rate, long-term follow-up, and mechanism are not well defined. METHODS AND RESULTS: This prospective study enrolled consecutive patients undergoing CABG at a single institution. Patients were followed up for the development of sustained VT, and a detailed analysis of clinical, angiographic, and surgical variables associated with the occurrence of VT was performed. A total of 382 patients participated, and 12 patients (3.1%) experienced >/=1 episode of sustained VT 4.1+/-4.8 days after CABG. In 11 of 12 patients, no postoperative complication explained the VT; 1 patient had a perioperative myocardial infarction. The in-hospital mortality rate was 25%. Patients with VT were more likely to have prior myocardial infarction (92% versus 50%, P<0.01), severe congestive heart failure (56% versus 21%, P<0.01), and ejection fraction <0.40 (70% versus 29%, P<0.01). When all 3 factors were present, the risk of VT was 30%, a 14-fold increase. Patients with VT had more noncollateralized totally occluded vessels on angiogram (1.4+/-0.97 versus 0.54+/-0.7, P<0.01), a bypass graft across a noncollateralized occluded vessel (1.50+/-1.0 versus 0.42+/-0.62, P<0.01), and a bypass graft across a noncollateralized occluded vessel to an infarct zone (1.50+/-1.0 versus 0.17+/-0.38, P<0.01). By multivariate analysis, the number of bypass grafts across a noncollateralized occluded vessel to an infarct zone was the only independent factor predicting VT. CONCLUSIONS: The first presentation of sustained monomorphic VT in the recovery period after CABG is uncommon, but the incidence is high in specific clinical subsets. Placement of a bypass graft across a noncollateralized total occlusion in a vessel supplying an infarct zone was strongly and independently associated with the development of VT.     

Right and left ventricular function after cardiac transplantation. Changes during and after rejection

BACKGROUND. Attempts to identify noninvasive markers of ventricular dysfunction accompanying acute rejection have been hampered by a lack of detailed simultaneous hemodynamic data. Therefore, we prospectively performed serial monitoring of detailed left and right heart hemodynamic parameters in cardiac transplant recipients at the time of routine endomyocardial biopsy to better define the physiology of the allograft heart during and after acute rejection. METHODS AND RESULTS. To better assess the pathophysiology of the rejection process, 18 cardiac transplant patients were prospectively studied by serial right heart micromanometer catheterization and digital image processing at the time of routine endomyocardial biopsy. Eleven patients had 18 episodes of rejection. Studies of baseline (negative biopsy preceding rejection), rejection (acute moderate rejection), and resolved (first negative biopsy after rejection) states were compared. Seven patients who did not experience an episode of rejection served as the control group. Right ventricular minimum and end-diastolic pressures increased from baseline values of 0.9 +/- 3.2 and 6.9 +/- 3.7 mm Hg, respectively, to 3.2 +/- 5.5 and 9.9 +/- 6.6 mm Hg, respectively, with rejection (both variables, p less than 0.05) and remained elevated despite histological resolution of rejection (4.3 +/- 5.5 and 10.0 +/- 7.1 mm Hg, respectively; p less than 0.05 for both variables compared with baseline values). Concurrently, right ventricular end-diastolic volumes (133 +/- 29, 119 +/- 27, and 114 +/- 30 ml; baseline, rejection, and resolved, respectively) and left ventricular end-diastolic volumes (133 +/- 24, 117 +/- 20, and 113 +/- 30 ml; baseline, rejection, and resolved, respectively) significantly decreased during rejection and remained decreased after resolution of rejection (rejection and resolved compared with baseline values, p less than 0.05). Right ventricular chamber stiffness (0.055 +/- 0.035, 0.085 +/- 0.057, and 0.092 +/- 0.076 mm Hg/ml; baseline, rejection, and resolution, respectively; rejection and resolved compared with baseline values, p less than 0.05) increased with rejection and remained elevated after resolution of rejection. Right ventricular peak filling rate also increased from a baseline value of 2.48 +/- 0.45 to 2.76 +/- 0.63 ml end-diastolic volumes per second with rejection (p less than 0.05). Elevation of right ventricular filling pressures, peak filling rate, and chamber stiffness with a concomitant decrease in end-diastolic volume is consistent with a restrictive/constrictive physiology. Mean arterial blood pressure and systemic vascular resistance were elevated after the resolution of rejection (compared with either rejection or baseline values, p less than 0.05) associated with a higher mean daily dose of prednisone (resolved compared with either baseline or rejection values, p less than 0.05). The control group experienced a time-dependent increase in mean and diastolic systemic arterial pressures (both comparisons, p less than 0.05) without detectable diastolic dysfunction. CONCLUSIONS. Persistence of biventricular diastolic dysfunction may be due to an irreversible effect of rejection, although multifactorial changes in left ventricular afterload occur that may complicate serial assessment of ventricular function.     

Hypoxic hepatitis in children after cardiac surgery

<正>To the Editor: Hypoxic hepatitis(HH), also known as ischemic hepatitis or shock liver, is a liver injury characterized by necrosis of centrilobular hepatocytes with a rapid increase in serum aminotransferase levels. The incidence rate of HH among patients in the intensive care unit(ICU) was found to be 0.9%-11.9% [1]. Occurrence of HH appears to have a significant impact on the clinical outcome.     

alpha-Adducin Gly460Trp polymorphism,left ventricular mass and plasma renin activity

OBJECTIVE: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. METHODS: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen and alpha-adducin polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. RESULTS: The alpha-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P= 0.006). Patients homozygous for the allele of that polymorphism had a LV mass index (123.4 +/- 10.5 g/m(2) ) significantly higher compared with heterozygotes (90.8 +/- 2.5 g/m(2) , P<0.01) or homozygotes (94.7 +/- 1.7 g/m(2) , P<0.05). These subjects also have significantly lower PRA (F = 4.2, P= 0.017). Albeit uncommon, 40% of homozygotes of the alpha-adducin polymorphism had LVH (odds ratio, 15.1; 95% confidence interval, 3.0-82.1). CONCLUSIONS: The homozygotic state of the allele of alpha-adducin polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.     

Glucagon stimulation of plasma renin activity in humans.

Administration of 0.2 mg of glucagon by intravenous bolus resulted in an increase in plasma renin activity (PRA) in 2 of 5 normal volunteers on their usual diet. Two of the nonresponders subsequently showed a PRA response to glucagon after sodium depletion. A lower dose of glucagon (0.01 mg) had no effect on PRA despite a 31 mg/100 ml rise in blood glucose and peak plasma glucagon of over 2000 pg/ml. In conclusion, glucagon can stimulate PRA but it is not a potent stimulator; its effect may be potentiated by sodium depletion.     

Changes in plasma renin activity and aldosterone concentration in response to endothelin injection in dogs

The effects of endothelin on the renin-aldosterone system were examined by injecting it intravenously at low (40 pmol/kg) and high (400 pmol/kg) doses into pentobarbital-anesthetized dogs. Plasma renin activity and aldosterone concentration together with hemodynamic parameters were measured before and 60 min after endothelin injection. The lower dose of endothelin induced no significant increase in mean blood pressure or total peripheral resistance. It caused a slight decrease of plasma renin activity from 10.3 +/- 1.6 to 5.9 +/- 1.3 micrograms.l-1.h-1 (p less than 0.1) and a decrease of aldosterone concentration from 364 +/- 68 to 231 +/- 58 ng/l (p less than 0.05) with an increase in total peripheral resistance (p less than 0.05), but it did not cause any clear change in the plasma renin activity or aldosterone concentration. Thus, endothelin increases the blood pressure mainly by vasoconstriction. The finding of a slight decrease in the plasma renin activity after the lower dose of endothelin, together with our previous finding that endothelin inhibits renin release from isolated rat glomeruli, suggests that endothelin inhibits renin release in vivo. With the higher dose of endothelin, stimulation of renin release secondary to renal vasoconstriction might have counteracted the direct inhibitory action of endothelin. The decrease in aldosterone concentration may have been due to the direct inhibitory action of endothelin on aldosterone release or it may be a secondary effect induced by suppression of plasma renin activity.