Using the World Wide Web--a new approach to risk identification of diabetes mellitus

We evaluated 30 consecutive patients and 48 age- and sex-matched controls to explore the possibility of a pathogenic contribution by plasma endothelin-1 in the cardiac expression of systemic sclerosis. Venous plasma endothelin-1 was measured by radio-immunoassay and left ventricular function by echocardiography. The patient group had elevated plasma endothelin-1 (2.6 +/- 0.2 vs. 1.8 +/- 0.1 pmol/1, P < 0.001), but endothelin-1 was not related to age, heart rate, blood pressure, total peripheral resistance, disease duration or systemic sclerosis score. Endothelin-1 was related to left ventricular hypertrophy in terms of septal thickness (r = 0.33, P < 0.01) and left ventricular mass index (r = 0.32, P < 0.01). Plasma endothelin-1 was further related to measures indicating reduced left ventricular filling; left atrial emptying index (r = -0.50, P < 0.0005), the first third filling fraction (r = -0.31, P < 0.05) and the time velocity integral of Doppler early/late filling velocity (r = -0.40, P < 0.001). Furthermore, circulating endothelin-1 was related to impaired left ventricular contractility as estimated by pre-ejection period/left ventricular ejection time (r = 0.32, P < 0.01) and end-systolic wall stress/volume index (r = -0.30, P < 0.05). We conclude that plasma endothelin-1 is elevated in relation to the degree of left ventricular hypertrophy, diastolic dysfunction and impaired contractility in systemic sclerosis. It may be of pathogenic importance to the cardiac involvement in systemic sclerosis which is not mediated via an increase in systemic blood pressure. It is not yet clear whether our findings are exclusive to systemic sclerosis patients or represent a generalized phenomenon in patients with impaired left ventricular function.     

Release of soluble tumour necrosis factor alpha receptors during and after paediatric cardiopulmonary bypass. Correlation with haemodynamic and clinical variables

The release of cytokines during cardiopulmonary bypass (CPB) may contribute to haemodynamic alternations encountered after open heart surgery. Regulatory mechanisms exist and include soluble cytokine receptors. We have measured blood levels of tumour necrosis factor (TNF) and its soluble receptor (TNFsr) during and after open heart surgery in children. Correlation analysis to haemodynamic and clinical variables was performed. Using immunoassays the authors registered a significant increase in plasma levels of TNFsr with peak levels 2 h post-operatively at a level of 1702 +/- 170 pg/ml. The concentration of TNFsr remained significantly elevated until 48 h postoperatively but TNF was not significantly elevated. An inverse correlation existed between peak TNFsr and mean arterial pressure (rho = -0.827, P < 0.05), between TNFsr and cardiac index (rho = -0.8, P < 0.05), between TNFsr and left ventricular stroke work index (rho = -0.983, P < 0.01), between TNFsr and weight (rho = -0.85, P < 0.05) and between TNFsr and body surface area (rho = -0.867, P < 0.05). The authors demonstrate that the smallest children experienced the highest TNFsr concentration post-operatively. Furthermore cardiac performance, expressed as cardiac index and left ventricular stroke work index, correlated inversely to peak TNFsr level post-operatively.     

Elderly patients in chronic hemodialysis: risk factors for left ventricular hypertrophy

In the past few years in Western countries, there has been an increasing proportion of elderly patients beginning renal replacement therapy. Left ventricular hypertrophy (LVH) is associated with an increased mortality rate due to cardiovascular disease, the main cause of death in patients on chronic hemodialysis. In this study, we evaluated 67 chronic hemodialysis patients older than 65 years (33 women and 34 men; mean age, 72.6 years; mean time on chronic hemodialysis, 51.3 months). Several biological and laboratory data were analyzed. The left ventricular mass was calculated using the Penn convention criteria. LVH was observed in 49 patients (73%). These 49 patients were divided into two groups (group 1, concentric hypertrophy, n = 22; and group 2, eccentric hypertrophy, n = 27) and compared with a control group (patients without LVH, n = 18). Group 1 (P = 0.06) and group 2 (P = 0.055) showed higher systolic blood pressures and group 2 showed a lower hematocrit (P = 0.024). The echocardiographic parameters were expectedly different: group 1 had higher posterior left ventricular wall thickness (P = 0.0001), interventricular septum thickness (P = 0.0001), and left ventricular wall relative thickness (P = 0.002), and group 2 had higher left ventricular end-diastolic diameter (P = 0.0001), interventricular septum thickness (P = 0.01), and posterior left ventricular wall thickness (P = 0.023). Using the left ventricular mass index as the dependent variable and the evaluated biological and laboratory data as the independent variables, we found in a stepwise multiple regression model that only systolic blood pressure (t = 3.430; P = 0.0011), age (t = 2.059; P = 0.044), interdialytic weight gain (t = 2.236; P = 0.029), and hematocrit (t = -1.961; P = 0.054) independently influenced the left ventricular mass index (R2 = 0.313; P = 0.0001). Further studies are needed to determine whether reduction of the left ventricular mass index, through control of blood pressure and correction of anemia, will decrease the cardiovascular events in this particular population.     

Augmentation of the cardiac natriuretic peptides by beta-receptor antagonism: evidence from a population-based study

OBJECTIVES: The present retrospective analysis of data derived from a population-based study examined the relationship between intake of beta-receptor antagonists and plasma concentrations of the cardiac natriuretic peptides and their second messenger. BACKGROUND: Beta-receptor antagonists are widely used for treatment of cardiovascular disease. In addition to direct effects on heart rate and cardiac contractility, recent evidence suggests that beta-receptor antagonists may also modulate the cross talk between the sympathetic nervous system and the cardiac natriuretic peptide system. METHODS: Plasma concentrations of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and their second messenger cyclic guanosine monophosphate (cGMP) were assessed in addition to anthropometric, hemodynamic and echocardiographic parameters in a population-based sample (n = 672), of which 80 subjects used beta-receptor antagonists. RESULTS: Compared to subjects without medication, subjects receiving beta-receptor antagonists were characterized by substantially elevated ANP, BNP and cGMP plasma concentrations (plus 32%, 89% and 18%, respectively, p < 0.01 each). Analysis of subgroups revealed that this effect was highly consistent and present even in the absence of hypertension, left atrial enlargement, left ventricular hypertrophy or left ventricular dysfunction. The most prominent increase was observed in a subgroup with increased left ventricular mass index. By multivariate analysis, a statistically significant and independent association between beta-receptor antagonism and ANP, BNP and cGMP concentrations was confirmed. Such an association could not be demonstrated for other antihypertensive agents such as angiotensin-converting enzyme inhibitors or diuretics. CONCLUSIONS: Beta-receptor antagonists appear to augment plasma ANP, BNP and cGMP concentrations. The current observation suggests an important contribution of the cardiac natriuretic peptide system to the therapeutic mechanism of beta-receptor antagonists.     

Prognostic value of arrhythmogenic markers in systemic hypertension

OBJECTIVE: To evaluate the prognostic value of arrhythmogenic markers in hypertensive patients. DESIGN: Two hundred and fourteen hypertensive patients without symptomatic coronary disease, systolic dysfunction, electrolyte disturbances or anti-arrhythmic therapy were included. Recordings were made of 12-lead standard ECGs with calculations of QT interval dispersion, 24 h Holter ECGs (204 patients), echocardiography (187 patients) and signal-averaged ECGs (125 patients). RESULTS: Baseline data: echocardiographic left ventricular hypertrophy was found in 63 patients (33.7%), non-sustained ventricular tachycardia (Lown class IV b) in 33 patients (16.2%), ventricular late potentials in 27 patients (21.6%). Mortality: after a mean follow-up of 42.4 +/- 26.8 months, global mortality was 11.2% (24 patients), cardiac mortality 7.9% (17 patients), sudden death 4.2% (nine patients). Univariate analysis: predictors of global, cardiac and sudden death were age > or = 65 years, ECG strain pattern, Lown class IV b and QT interval dispersion > 80 ms (P < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (P = 0.002). Multivariate analysis: only Lown class IV b was an independent predictor of global (RR 2.6, 95% CI 1.2-6.0) and cardiac mortality (RR 3.5, 95% CI 1.2-9.7). CONCLUSION: In hypertensive patients, non-sustained ventricular tachycardia has a prognostic value.     

Reversal of left ventricular hypertrophy in essential hypertension. A meta-analysis of randomized double-blind studies

OBJECTIVE: To determine the ability of various antihypertensive agents to reduce left ventricular hypertrophy, a strong, blood pressure-independent cardiovascular risk factor, in persons with essential hypertension. DATA SOURCES: MEDLINE, DIMDI, RINGDOC, ADES, EMBASE, and review articles through July 1995 (English-language and full articles only). STUDY SELECTION: Meta-analysis of all published articles including only double-blind, randomized, controlled clinical studies with parallel-group design. DATA EXTRACTION: Intensive literature search and data extraction according to a prefixed scheme performed independently by 2 investigators. Reduction of left ventricular mass index after antihypertensive therapy with placebos, diuretics, beta-blockers, calcium channel blockers, or angiotensin-converting enzyme (ACE) inhibitors was the principal parameter. DATA SYNTHESIS: Of 471 identified references describing the effects of antihypertensive drugs on left ventricular hypertrophy, only 39 clinical trials fulfilled the inclusion criteria of our study. We found that the decrease in left ventricular mass index was more marked the greater was the decline in blood pressure (systolic r=0.46, P<.001; diastolic r=0.21, P=.08) and the longer was the duration of therapy (r=0.38, P<.01). After adjustment for different durations of treatment (mean duration of treatment, 25 weeks), left ventricular mass decreased 13% with ACE inhibitors, 9% with calcium channel blockers, 6% with beta-blockers, and 7% with diuretics. There was a significant difference between drug classes (P<.01): ACE inhibitors reduced left ventricular mass more than beta-blockers (significant, P<.05) and diuretics (tendency, P=.08). Similar differences between drug classes were found with regard to effect on left ventricular wall thickness (P<.05). CONCLUSIONS: The database of articles published through July 1995 is small and incomplete, and most of the articles are of poor scientific quality. In this first meta-analysis including only double-blind, randomized, controlled clinical studies, decline in blood pressure, duration of drug treatment, and drug class determined the reductions in left ventricular mass index. The ACE inhibitors seemed to be more potent than beta-blockers and diuretics in the reduction of left ventricular mass index; calcium channel blockers were somewhat in the intermediate range. The ACE inhibitors and, to a lesser extent, calcium channel blockers emerged as first-line candidates to reduce the risk associated with left ventricular hypertrophy.     

Comparison of angiotensin converting enzyme and renin inhibition in rats following myocardial infarction

Renal and systemic hemodynamics were studied in rats 1 month after induction of myocardial infarction by ligation of the left coronary artery. The mean arterial pressure, heart rate, and cardiac index were not different from controls, but there were striking elevations in heart weight (p < 0.001), left ventricular end diastolic pressure (p < 0.002), and renal vascular resistance (p < 0.01). Renal blood flow and the percent of cardiac output perfusing the kidneys were reduced by 18% (p < 0.01) and 14% (p < 0.01), respectively. Acute angiotensin inhibition was studied at a dose of the converting enzyme inhibitor, enalapril, or the renin inhibitor, CP71362, that lowered the mean arterial pressure by 15 mm Hg in normal rats. In normal rats, enalapril and CP71362 were without effect on renal blood flow (RBF), renal vascular resistance (RR), and RBF as a percent of cardiac output. However, in rats with myocardial infarction, enalapril and CP71362 increased the RBF and RBF as a percent of cardiac output and lowered the RR to levels similar to normal controls (p < 0.02). Enalapril and CP71362 were equally effective in reducing the left ventricular end-diastolic pressure and total peripheral resistance in rats with myocardial infarction. These data demonstrate significant intrarenal vasoconstriction following myocardial infarction in the absence of detectable changes in mean arterial pressure or cardiac index. Converting enzyme inhibition or renin inhibition had similar beneficial effects on cardiorenal function, suggesting that both classes of compounds act by a similar mechanism to improve renal hemodynamics in congestive heart failure.     

Short and long-term cardiovascular effects of growth hormone therapy in growth hormone deficient adults

OBJECTIVE: Since GH substitution therapy is now available for adult GH deficient patients, information on the cardiovascular effects of GH substitution has assumed major clinical interest. We have therefore assessed cardiovascular effects of short and long-term growth hormone substitution therapy in these patients. PATIENTS AND MEASUREMENTS: Doppler echocardiography was performed in 21 GH deficient patients after 4 months placebo and 4 months GH therapy, in a double blind cross-over study. In an open design study, 13 patients were reinvestigated following 16 months and 9 patients following 38 months of GH therapy. Twenty-one age and sex-matched normal control subjects were also investigated. RESULTS: Heart rate was increased in placebo treated patients as compared to controls. After 4 months of GH treatment, heart rate showed a further increase (10%, P < 0.01) and seemed to remain elevated after 16 months of GH therapy. Systolic and diastolic blood pressures were significantly lower in placebo treated patients than in controls, and did not change significantly after GH treatment. The left ventricular diastolic diameter was reduced in patients as compared to controls, but increased after 4 months GH therapy (P > 0.05) and seemed to increase further during prolonged GH treatment. Cardiac index was at the same level in controls and in placebo-treated patients, but increased by 20% following GH therapy and remained elevated after 16 and 38 months (P < 0.05) of GH substitution. CONCLUSION: Following GH substitution in GH deficient adult patients, left ventricular diastolic dimensions increased and seemed to normalize, while heart rate and cardiac output were found to be increased to supranormal levels.     

An investigation of the placebo effect and age-related factors in the report of needle pain from venipuncture in children

Reversal of left ventricular hypertrophy has been shown to improve left ventricular diastolic function in elderly patients with hypertension, but little is known about whether this affects physical performance. Left ventricular mass, cardiac function at rest and during submaximal exercise, and physical performance were assessed in 38 elderly patients with hypertension with left ventricular hypertrophy and normal systolic function before and after 8 and 14 months of therapy with amlodipine or hydrochlorothiazide or both. Blood pressure control was achieved with amlodipine in 18 patients, with hydrochlorothiazide in seven, and with the combination of these drugs in 13. Left ventricular mass index was similarly reduced from approximately 150 to approximately 100 g/m2 at 14 months' in each treatment group. Systolic function was maintained with the three treatment regimens, whereas similar decreases in time to peak filling rate and increases in first-third filling fraction occurred both at rest and during submaximal exercise after 8 months and further after 14 months of therapy. Exercise capacity did not significantly change in the group as a whole, but individual changes in peak oxygen uptake at the end of treatment correlated significantly with the decrease in time to peak filling rate during submaximal exercise (r = -0.49; p < 0.01). It is concluded that long-term blood pressure control with amlodipine or hydrochlorothiazide or both is associated with significant reductions in left ventricular mass and improved diastolic function in elderly patients with hypertension with left ventricular hypertrophy. Despite this reduction in left ventricular mass, left ventricular systolic function and physical performance are well preserved during submaximal exercise.     

Superiority of brain natriuretic peptide as a hormonal marker of ventricular systolic and diastolic dysfunction and ventricular hypertrophy

Atrial and brain natriuretic peptides (ANP and BNP) are produced by the heart, and their plasma concentrations are increased in human chronic congestive heart failure. Although separate studies have suggested that circulating levels of the biologically active C-terminal ANP, the biologically inactive N-terminal ANP, and BNP may have diagnostic utility in the detection of left ventricular systolic dysfunction or left ventricular hypertrophy, no studies have directly assessed the relative value of these peptides prospectively. We therefore designed this study to compare the relative ability of the different natriuretic peptides to detect abnormal left ventricular systolic and diastolic function and left ventricular hypertrophy. Using a prospective study design, we investigated 94 patients referred for cardiac catheterization and 15 age-matched normal subjects. The diagnostic abilities of elevated plasma C-terminal ANP, N-terminal ANP-(1-30), and BNP concentrations to identify systolic dysfunction (ejection fraction < 45%), diastolic dysfunction (time constant of left ventricular relaxation > 55 milliseconds, left ventricular end-diastolic pressure > 18 mm Hg), and left ventricular hypertrophy (left ventricular mass index > 120 g/m2) were objectively compared by receiver operating characteristic analysis. The areas under the receiver operating characteristic curve of BNP for detecting each of these abnormalities ranged from 0.715 to 0.908 and were significantly greater than those of C-terminal ANP or N-terminal ANP-(1-30). The sensitivity and specificity of an elevated plasma BNP, which we defined as greater than the mean + 3 SD of the 15 age-matched normal subjects, were 0.83 and 0.77, respectively, for detecting ejection fraction less than 45%, 0.85 and 0.70 for detecting the time constant of left ventricular relaxation greater than 55 milliseconds, 0.63 and 0.76 for detecting left ventricular end-diastolic pressure greater than 18 mm Hg, and 0.81 and 0.85 for detecting left ventricular mass index greater than 120 g/m2. The use of BNP and one other peptide increased sensitivity (0.90 to 0.96), albeit with lower specificity (0.56 to 0.71). An elevated plasma BNP was a more powerful marker of left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and left ventricular hypertrophy than C-terminal ANP or N-terminal ANP-(1-30) in this population of patients with suspected cardiac disease. Measurement of BNP alone or in combination with C-terminal ANP or N-terminal ANP-(1-30) has potential utility for the detection of altered left ventricular structure and function in a patient population at risk for cardiovascular disease.     

Surgical repair of fecal incontinence. Correlation of sonographic anal sphincter integrity with subjective cure

We examined the relationship between left ventricular hypertrophy (LVH) and renal and retinal damage in 174 untreated patients with essential hypertension. As an index of renal and retinal damage, we examined proteinuria and retinal vascular change. LVH was diagnosed according to left ventricular mass obtained from echocardiography. Of the hypertensive patients, 111 patients (64%) had LVH. The incidences of proteinuria and advanced retinal vascular change were higher in patients with LVH than in those without LVH. In a multiple regression model, there was a significant positive correlation between left ventricular mass and proteinuria, as well as diastolic blood pressure, sex, age and body mass index. In conclusion, proteinuria is related to elevated left ventricular mass in patients with essential hypertension.     

Prognostic value of ventricular arrhythmia in hypertensive patients

OBJECTIVE: Hypertensive left ventricular hypertrophy (LVH) is associated with increased risk of arrhythmias and mortality. However, no clinical study demonstrated a significant relation between ventricular arrhythmias and mortality in systemic hypertension. DESIGN AND METHODS: To evaluate the prognostic value of arrhythmogenic markers in systemic hypertension, we included between 1987 and 1993. 214 hypertensive patients, 59.1 +/- 12.8 years old, without symptomatic coronary disease, myocardial infarction, systolic dysfunction, electrolyte disturbances or antiarrhythmic therapy. At inclusion, an ECG, a 24 h Holter ECG (204 patients) with Lown classification of ventricular arrhythmias, an echocardiography (reliable in 187 patients) with left ventricular mass index and ejection fraction calculation, a SAECG (125 patients, enrolled after 1988) with ventricular late potentials (LP) were recorded. QT interval dispersion (QTd) was calculated on 12 leads standard ECG and LVH was appreciated. RESULTS: At baseline echocardiographic LVH was recorded in 63 patients (33.7%) with normal ejection fraction (75 +/- 7.4%). Non-sustained ventricular tachycardia (Lown IVb) was found in 33 pts (16.2%) and LP in 27 patients (21.6%). After a mean follow up of 42.4 +/- 26.8 months, all-cause mortality was 11.2% (24 patients); 17 patients died of cardiac causes (7.9%); of these 9 patients (4.2%) died suddenly. In univariate analysis, age, strain pattern of LVH, advanced Lown classes and abnormal QT dispersion (> 80 ms) were significantly related to global, cardiac and sudden death (p < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (p = 0.002). LP failed to predict mortality. In multivariate analysis, only Lown class IVb was an independent predictor of global and cardiac mortality, increasing the risk of global death 2.6 fold [1.2-6.0] (CI 95%) and the risk of cardiac death 3.5 fold [1.2-9.7] (CI 95%). CONCLUSIONS: In hypertensive patients the presence of non-sustained ventricular tachycardia on 24 h Holter has a prognostic value.     

Cardiac manifestations of primary hypothyroidism. Determinant factors and treatment response

INTRODUCTION AND OBJECTIVES: Previous studies have not fully established the magnitude and determinant factors of cardiac manifestations of primary hypothyroidism. This study was aimed to assess the effects of thyroid deficiency on cardiac performance and structure. PATIENTS AND METHODS: We studied by echocardiography 19 patients with overt and 23 with subclinical hypothyroidism, and 21 control subjects. Patients were restudied one year after L-thyroxine therapy. Systolic function was assessed by the observed/predicted fractional shortening ratio. The predicted fractional shortening was calculated from the inverse relation of fractional shortening to end-systolic stress (p < 0.0001) in normal subjects. RESULTS: The observed/predicted fractional shortening ratio was lower (p = 0.043) and left ventricular mass was higher (p = 0.028) in overt hypothyroidism than in subclinical hypothyroidism and control subjects. By multivariate analysis, fractional shortening ratio was related to thyroxine levels (p = 0.0002), systemic vascular resistance (p = 0.0001) and age (p = 0.0009), and left ventricular mass was related to thyroxine levels (p = 0.0004) and weight (p = 0.0001). Pericardial effusion was observed in 37% of patients with overt hypothyroidism and 9% of patients with subclinical hypothyroidism (p = 0.03), and was mainly related to TSH levels (p = 0.0098). Hormone replacement therapy increased systolic function in overt hypothyroidism. Left ventricular mass did not change after therapy. Pericardial effusion disappeared in all patients. CONCLUSIONS: Primary hypothyroidism produces a decrease in myocardial contractility and an increase in left ventricular mass, both related to the severity of hormone deficiency. Pericardial effusion is mainly related to thyrotrophin plasma levels. Most of cardiac manifestations of hypothyroidism reverse with L-thyroxine therapy.     

Single-drug therapy and reduction of left ventricular mass in hypertension

Echocardiography has provided most of what is understood today about the relationships between human hypertension, cardiac anatomic and functional responses. It has proven its value in determining the effects of antihypertensive therapy on cardiac structure and function. A growing body of research supports initial concerns that not all drugs effective for blood pressure reduction are effective for reduction of left ventricular mass and regression of LVH. It has been of interest that agents initially believed to be ineffective for left ventricular mass reduction (principally diuretics and beta blockers) on the basis of pathophysiological theory and inadequate clinical trials, may in fact be quite effective for LVH regression, as well as improved cardiac outcomes. Hence, supposed inefficacy of these agents for this purpose should no longer be used as a reason to disregard long-standing recommendations of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of Hypertension supporting the use of diuretics and beta blockers for the initial pharmacotherapy of hypertension.     

Association between blood pressure and circulating hormonal factors with left ventricular mass in patients with essential hypertension older than 55 years of age

BACKGROUND: The prevalence of left ventricular hypertrophy (LVH) is higher in elderly patients with hypertension than in normotensive patients. The factors relationed herewith are not well known. The first purpose was to analyse the relationship between the levels of blood pressure (BP) recorded by ambulatory blood pressure monitoring (ABPM) and the left ventricular mass index (LVMI) in a group of untreated patients older than 55 years with essential hypertension. Our second purpose was to observe the relationship between the concentration of several circulating hormones and the left ventricular mass index. SUBJECTS AND METHODS: The study included 31 untreated patients with mild to moderate essential hypertension and 37 healthy normotensives. Both groups were of similar age, sex and body mass index. We determined for both groups the casual arterial pressure (CAP), ambulatory BP monitoring (ABPM) throughout 24 h, daytime (07.00-23.00 h), nighttime (23.00-07.00 h), left ventricular mass index (LVMI) (following Devereux's formula) and circulating levels of endothelin-1, aldosterone, renine, free adrenaline and noradrenaline. RESULTS: The ILVM in hypertensive patients was 139.6 +/- 35.9 g/m2 and in 124.0 +/- 31.8 g/m2 in normotensive (p < 0.05). The percentage of patients with LVH was 63 and 43%, respectively (p < 0.05). The LVMI in hypertensive patients was correlated with the diastolic CAP (97 +/- 7 mmHg) (r = 0.41; p < 0.05), unlike with the systolic CAP (164 +/- 18 mmHg). The ILVM in normotense patients was not associated neither with the systolic CAP (126 +/- 10 mmHg) nor with the diastolic (79 +/- 6 mmHg). In hypertensive patients we found a slight association between the LVMI and the systolic ABPM (130 +/- 14 mmHg) during nighttime (r = 0.41; p < 0.05). The rest of average ambulatory BP and the hormonal values at study did not show a correlation with the LVMI in both groups. CONCLUSIONS: A slight correlation exists between BP (casual and determined with ambulatory blood pressure monitoring throughout 24 hours) and the left ventricular mass index in mild to moderate untrated hypertensive patients older than 55 years. We did not observe correlations between the circulating levels of endothelin-1, renin, aldosterone, free adrenaline and noradrenaline and the left ventricular mass. The average ventricular mass and the number of subjects with ventricular hypertrophy was significantly increased in hypertensives than in normotensives.     

Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients

We investigated the atrial (ANP) and brain natriuretic peptides (BNP), catecholamines, heart rate, and blood pressure responses to graded upright maximal cycling exercise of eight matched healthy subjects and cardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP (15.2 +/- 3.7 vs. 4.4 +/- 0.8 pmol/l; P < 0.01) and BNP (14.3 +/- 2. 6 vs. 7.4 +/- 0.6 pmol/l; P < 0.01), were elevated in HTR, but catecholamine levels were similar in both groups. Peak exercise O2 uptake and heart rate were lower in HTR. Exercise-induced maximal ANP increase was similar in both groups (167 +/- 34 vs. 216 +/- 47%). Enhanced BNP increase was significant only in HTR (37 +/- 8 vs. 16 +/- 8%; P < 0.05). Similar norepinephrine but lower peak epinephrine levels were observed in HTR. ANP and heart rate changes from rest to 75% peak exercise were negatively correlated (r = -0.76, P < 0.05), and BNP increase was correlated with left ventricular mass index (r = 0.83, P < 0.01) after heart transplantation. Although ANP increase was not exaggerated, these data support the idea that the chronotropic limitation secondary to sinus node denervation might stimulate ANP release during early exercise in HTR. Furthermore, the BNP response to maximal exercise, which is related to the left ventricular mass index of HTR, is enhanced after heart transplantation.     

Aging and regression of cardiac hypertrophy in the hypertensive patient

OBJECTIVE: This study was aimed at determining factors acting on the regression of left ventricular hypertrophy due to essential hypertension. METHODS: It was a non-randomized, echocardiographic study of 60 previously untreated hypertensive subjects (20 to 75 years of age). RESULTS: Following a 5-year therapy, the decrease in the left ventricular mass was 14%. Normalization of blood pressure and reversal of left ventricular hypertrophy were obtained in 50% and 58% of patients, respectively. Patients of the non-responder group (non-response being defined as a less than 10% decrease in the left ventricular mass) were older and had a longer history of high blood pressure. A positive correlation was observed between age and decrease in the left ventricular mass, the latter being less marked in older patients. Antihypertensive drugs classes had no influence on reversal of left ventricular hypertrophy. CONCLUSION: Ageing may be a factor of resistance to the decrease in left ventricular mass with therapy. These results suggest that early screening and management of hypertension are essential.     

Relation of exercise-induced myocardial ischemia to cardiac and carotid structure

There is a strong relation of carotid atherosclerosis to coronary artery disease and left ventricular hypertrophy. In addition, abnormalities of carotid structure are strongly associated with abnormal left ventricular geometry and structure. However, little is known regarding the relation of exercise-induced ST depression to carotid atherosclerosis, carotid, or left ventricular structure in the absence of apparent coronary disease. The relationship of exercise ECG myocardial ischemia to the presence of carotid atherosclerosis and to carotid and left ventricular structure was assessed in 204 asymptomatic subjects free of clinical evidence of cardiovascular disease. Myocardial ischemia on the exercise ECG, defined by a chronotropically adjusted ST/HR slope of >3.47 microV/bpm, was associated with a nearly threefold greater likelihood of discrete carotid atherosclerosis (50% [6 of 12] versus 17% [29 of 192], P=.007) and with older age, male sex, higher systolic and diastolic blood pressures, greater left ventricular mass and mass index, and greater common carotid artery intimal-medial thickness and cross-sectional area index. Stepwise logistic regression analyses, including standard risk factors, revealed that only carotid artery cross-sectional area index (P=.0007) and systolic blood pressure (P=.005) independently predicted an abnormal chronotropically adjusted ST/heart rate slope. Moreover, among 132 subjects with > or = 10 microV of ST-segment depression, only left ventricular mass index and carotid artery cross-sectional area index were significant predictors of the chronotropically adjusted ST/heart rate slope response. Subendocardial ischemia on the exercise ECG is strongly associated with the presence of carotid atherosclerosis and is related to systolic blood pressure, carotid artery cross-sectional area index, and left ventricular mass index, independent of age, sex, and other cardiac risk factors. These findings provide additional insights into the relation between coronary and carotid atherosclerosis and suggest that an association among ischemia and left ventricular and carotid structural abnormalities may contribute to the pathogenesis of coronary events.     

Clinical polymorphic presentation and natural history of active myocarditis: experience in 60 cases

Eight-hundred thirty patients (pts) with suspected myocardial disease of undefined etiology were observed from 1978 to 1996. In 350 pts, the clinical diagnosis was of dilated cardiomyopathy (DCM) or myocarditis. An endomyocardial biopsy was performed on all patients and in 54 of them (15%), an active myocarditis was identified. In six cases, myocarditis was detected at autopsy. There were 37 male patients and 23 females, with an average age of 35.5 +/- 15 years (range 1.67). Mean time interval between clinical onset and diagnosis was 4 +/- 10 months. Clinical presentation was characterized in 4 cases by fulminant myocarditis (Group I), in 8 cases by chest pain (Group II), in 14 cases by arrhythmia (Group III: hypokinetic in 9 pts and hyperkinetic in 5) and, in the last 34 pts, by congestive heart failure (CHF) (Group IV). Improvement was defined at 9 +/- 3 months according to a clinical score based on left ventricular shortening fraction (increase > or = 5 units), New York Heart Association Class improvement by (at least one Class) and left ventricular end-diastolic diameter (decrease > or = 10%). The main clinical and instrumental parameters characterizing the groups were: a more severe dilatation and left ventricular dysfunction in the pts belonging to Group I or IV with respect to those in Group II and III; a significantly worse prognosis in terms of evolution in DCM or death/cardiac transplantation (CT) in the pts from the Group II and III. After a follow-up period of 48 +/- 46 months, the mortality in the four groups was: 100% (4/4), 0% (0/8), 21% (3/14), 38% (13/34). Fifty percent of deaths were concentrated in the first 2 years of follow-up. Left ventricular end-diastolic diameter (OR 1.09, p < 0.05), age (OR 0.95), presence of left ventricular bundle branch block (OR 2.32), right ventricular function (OR 2.43) at clinical onset and the status of improvement at 9 +/- 3 months of follow-up (OR 0.24, p < 0.05) are predictors of evolution in DCM or death/CT for the pts with onset from CHF (Group IV). Immunosuppressive treatment has been utilized for the 76% of the pts. No conclusion can be drawn on the efficacy of this therapy, but no adverse events significantly related to therapy have been observed in a 9 +/- 3 months follow-up period. In conclusion, myocarditis can show a clinical presentation polymorphism, which influences the prognosis and natural history of the disease. Evolution in DCM and adverse events (death/CT) are more common in Groups I and IV. Some simple parameters evaluated at clinical presentation and the proposed classification as "improved" or "not improved" after a short-term follow-up (9 +/- 3 months) show good predictive accuracy. The present study does not allow us to draw any conclusion about the efficacy of immunosuppressive treatment. A randomized, controlled, large-scale trial, with adequate follow-up and advanced histological diagnosis techniques will help define the role of immunosuppressive therapy and patient eligibility criteria for this treatment.     

Ventricular tachycardia revealing viral myocarditis

BACKGROUND: The first diagnostic hypothesis in a middle-aged patient presenting with inaugural ventricular tachycardia would be coronary artery disease. If the work-up lacks arguments for this etiology, other cardiac conditions may be involved (dilated cardiopathy, hypertrophic cardiopathy, valve disease arrhythmogenic dysplasia, long QT...). CASE REPORT: A 52-year-old male patient was referred for inaugural ventricular tachycardia. The initial work-up including echocardiography, coronography and the electrophysiologic study provided no explanation. The ventricular tachycardia was later attributed to viral myocarditis. DISCUSSION: Viral myocarditis should always be entertained in patients with unexplained ventricular tachycardia, particular if a viral context is present. In such cases, antibody-labeled scintigraphy is the choice exploration. This noninvasive technique provides determining diagnostic information and helps orient patient management.