Evaluation of long-term prognosis in patients with heart failure: is cardiac imaging with iodine-123 metaiodobenzylguanidine useful?

The effect of cardiac sympathetic activity on long-term prognosis in patients with heart failure was evaluated by cardiac imaging with iodine-123 metaiodobenzylguanidine (123I-MIBG) in 46 patients admitted for the first episode of heart failure (idiopathic dilated cardiomyopathy: 18, ischemic heart disease: 10, hypertensive heart disease: 7, valvular heart disease: 4, others: 7). Cardiac imaging was performed with 123I-MIBG and thallium-201 (201Tl) at rest on separate days before discharge. Using whole body imaging, the ratio of cardiac uptake of the isotope to total injected dose was calculated (percentage uptake). The cardiac uptake ratio of 123I-MIBG (percentage uptake of 123I-MIBG divided by percentage uptake of 201Tl) and percentage washout of 123I-MIBG from the heart over 3 hours were calculated as scintigraphic parameters. Cardiac events were defined as cardiac death or deterioration of heart failure requiring readmission. Scintigraphic parameters, clinical parameters, left ventricular function obtained by echocardiography and neurohumoral parameters were compared between the event group and event-free group. During the follow-up period of 26.9 +/- 13.9 (7.1-53.8 months), cardiac events developed in 14 patients (cardiac death in 10 and deterioration of heart failure in 4; 30%). Univariate analysis showed uptake ratio and washout rate of 123I-MIBG, percentage uptake of 201Tl, New York Heart Association class at discharge, fractional shortening of the left ventricle, serum norepinephrine and atrial natriuretic peptide levels differed significantly between the two groups. Cox proportional-hazard analysis showed that the uptake ratio was an independent predictor of cardiac events (p < 0.0001). When a cut-off point in the uptake ratio equal to or less than 0.50 and age equal to or more than 65 years old were included in the Cox proportional-hazard analysis instead of actual numbers, relative risks of cardiac events by each index were 31.2 (95% confidence interval, 3.9 to 247.6; p = 0.001) and 4.2 (p = 0.025), respectively. These data suggest that cardiac uptake of 123I-MIBG is a strong and independent predictor of long-term prognosis in patients with heart failure.     

Differential responsiveness of murine T lymphomas to local growth and invasion factors may determine metastasis formation in the ovaries

Iodine-123-metaiodobenzylguanidine [123I-MIBG] has been used to evaluate the cardiac sympathetic nervous system. We evaluated the effect of pulmonary hypertension on the sympathetic neuronal function of the left ventricle in patients with pulmonary hypertension. We studied 20 patients with either chronic lung disease or pulmonary vascular disease. The patients were divided into a pulmonary hypertensive group and a control group. Single photon emission tomography was performed in the resting state 15 min and 4 h after administration of 123I-MIBG. Regions of interest (ROI) were set in the left ventricular (LV) free wall, the interventricular septum (IVS) and outside the LV free wall on short-axis images. The washout rate and the ROI/LV uptake ratio were calculated in each ROI. The IVS:LV uptake ratio was significantly lower in the pulmonary hypertensive group than in the control group. Our results suggest that left heart sympathetic neuronal dysfunction initially occurs in the IVS before it involves the LV free wall subsequently.     

A case of hypertensive hypertrophy in which both regression of hypertrophy and improvement of the abnormalities in iodine-123-metaiodobenzylguanidine (MIBG) myocardial imagings were observed after antihypertensive therapy

A case of hypertensive hypertrophy is described in which both regression of hypertrophy and improvement of the abnormalities in iodine-123-metaiodobenzylguanidine (MIBG) myocardial imagings were seen after 7 months of antihypertensive therapy. A 58-year-old man was diagnosed as having essential hypertension and hypertensive hypertrophy. The patient was treated with antihypertensive drugs and showed regression of left ventricular hypertrophy on electrocardiograms and echocardiograms. MIBG observations made before and after antihypertensive therapy showed increased heart-to-mediastinum activity ratio and decreased cardiac washout ratio. Despite the many theories addressing the mechanisms of regression of left ventricular hypertrophy, the process is still unclear. In the present case, the improvement of cardiac sympathetic nervous dysfunction might have been related to the regression of left ventricular hypertrophy because the abnormality in MIBG images improved. MIBG, therefore, may be helpful in clarifying the mechanisms of the regression of hypertensive hypertrophy.     

Scientific challenges in environmental carcinogenesis

Myocardial uptake of iodine-123 meta-iodobenzylguanidine (123I-MIBG) was measured using scintigrams at rest in 12 patients with isolated, nonischemic mitral regurgitation (MR; regurgitant fraction 64% +/- 7%) and was related to the left ventricular (LV) function assessed by cardiac catheterization. Iodine-123 meta-iodobenzylguanidine activity in the upper mediastinum, liver, and lung was comparable between MR and control (n = 8) patients. The heart-to-mediastinum 123I-MIBG activity ratio 4 hours after injection was significantly (p < 0.01) decreased in MR (2.0 +/- 0.1, mean +/- SE) compared with control (2.7 +/- 0.1) with the increased clearance of MIBG. In addition, MR patients had significantly greater heterogeneity in the 123I-MIBG distribution within the myocardial images (26.1% +/- 2.1% intraimage variability for MR versus 15.6% +/- 0.8% for control, p < 0.01). Myocardial 123I-MIBG activity correlated positively with cardiac index and negatively with pulmonary capillary wedge pressure and LV volume indexes. Thus, 123I-MIBG scintigrams can be a noninvasive method for assessing the contractile dysfunction in MR.     

Managed care and outcomes of hospitalization among elderly patients with congestive heart failure

123I-radiolabeled metaiodobenzylguanidine (123I-MIBG) cardiac imaging has been used to evaluate the distribution of sympathetic nervous system (SNS) in the heart. Different heart diseases have shown impaired cardiac SNS distribution as reflected by MIBG activity. The aim of this study was to assess the cardiac distribution of SNS in normal subjects, using MIBG imaging. Ten normal subjects (1 male and 9 females, mean age 46 +/- 9 years) with no cardiac abnormalities underwent myocardial 123I-MIBG scintigraphy, Tc-99m methoxyisobutylisonitrile (MIBI) cardiac perfusion imaging and equilibrium radionuclide angiography (RNA). Regional myocardial MIBG and MIBI activities were quantitatively evaluated using a region of interest analysis. For this purpose, the left ventricle was divided into 6 myocardial regions as anterior, apical, inferior, septum, lateral and posterolateral. In particular, myocardial MIBG and MIBI activities were measured as myocardium to mediastinum ratio. Regional left ventricular function was assessed by RNA. Myocardial MIBG uptake was homogeneous in anterior (2.2 +/- 0.5), inferior (2.5 +/- 0.7), septal (2.4 +/- 0.4), lateral (2.3 +/- 0.4), and posterolateral (2.3 +/- 0.4) regions. Conversely, MIBG uptake was significantly lower in the apical region (1.9 +/- 0.3) compared to all other left ventricular segments (p < 0.05). Regional myocardial perfusion, as measured by MIBI uptake, was homogeneous in all regions. No regional left ventricular wall motion abnormalities were observed by RNA. In conclusion, our data suggest that a decreased MIBG uptake may be observed in the left ventricular apical region of normal subjects reflecting reduced sympathetic innervation of the apex. This finding is not related to myocardial perfusion or wall motion abnormalities. The knowledge of cardiac sympathetic innervation in normal subjects may be helpful to assess SNS abnormalities in heart disease.     

Dental fear with and without blood-injection fear: implications for dental health and clinical practice

BACKGROUND: It has been suggested that the sympathetic nervous system might play an important role in the development of coronary artery spasm. However, no cardiac imaging modality has been able to demonstrate abnormal sympathetic innervation in patients with coronary artery spasm. The purpose of this study was to assess the presence and location of abnormal sympathetic innervation using iodine 123-metaiodobenzylguanidine (123I-MIBG) single photon emission computed tomography (SPECT) and to evaluate the clinical efficacy of 123I-MIBG SPECT as a noninvasive screening test in patients with coronary artery spasm. METHODS AND RESULTS: Coronary arteriography and a provocative test with intravenous administration of ergonovine maleate were performed in 26 patients (20 men, 6 women, mean age 48.2+/-12.0 years, range 20 to 67 years) who were suspected of having a coronary artery spasm. The subjects were divided into 2 groups: group 1 (n = 18) comprised subjects with a positive provocative test result, and group 2 (n = 8) comprised subjects with negative provocative test results. Ten healthy subjects served as controls. No abnormal MIBG uptake was observed in the control subjects. Abnormal sympathetic nervous innervation using 123I-MIBG SPECT was observed either as a reduced uptake or a defective pattern in the perfused areas in 13 of the 18 regions supplied by vessels of ergonovine-induced vasospasm. Normal sympathetic innervation, as evidenced by normal 123I-MIBG uptake, was noted in all of the 60 segments of normal vessel territories. Reduced uptake of 123I-MIBG was not detected in the perfused areas of 5 vasospasm-induced vessels (perfusion territory of left anterior descending coronary artery [LAD] and the right coronary artery [RCA] in 2 and 3 patients, respectively). The sensitivity and specificity of 123I-MIBG for detection of coronary artery spasm were 72.2% (95% confidence interval [CI] 55% to 89%) and 100%, respectively. The positive predictive and negative predictive values were 100% and 92.3% (95% CI 91% to 93%), respectively. CONCLUSION: 123I-MIBG SPECT is a feasible method to evaluate noninvasively and localize the territories of coronary arteries with spasm. Invasive diagnostic coronary arteriography with ergonovine provocation test may be unnecessary for diagnosis of coronary artery spasm in patients with typical resting pain, negative exercise test or normal thallium perfusion scan results, but showing abnormalities in 123I-MIBG SPECT.     

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.     

Aldosterone levels and cardiac hypertrophy in professional cyclists

Aldosterone has been associated with the development of cardiac hypertrophy and a correlation has been found between levels of aldosterone and the degree of cardiac hypertrophy in hypertensive patients. Our study aimed to test the relation between physiologic cardiac hypertrophy and serum aldosterone in a group of highly trained cyclists. Determination of the left ventricular mass index (LVMI) was performed in a group of 40 professional cyclists by using Devereux's formula with correction for body surface area. After an overnight fast, blood samples were collected and serum aldosterone levels were measured using RIA. LVMI and serum aldosterone were intercorrelated using linear regression analysis. Twenty-three of the 40 cyclists (58%) presented an LVMI > 130 g.m-1 and the other 17 subjects (42%) presented an LVMI < 130 g.m-1. Serum aldosterone levels did not correlate with LVMI in either of the groups (LVMI > 130 g.m-1, r = -0.089; LVMI < 130 g.m-1, r = 0.146). The lack of correlation of this hypertrophy with serum aldosterone levels suggests that physiologic hypertrophy of the athlete's heart could be caused by a different stimulus to that seen in pathologic hypertrophy of hypertensives.     

Cardiac death prediction and impaired cardiac sympathetic innervation assessed by MIBG in patients with failing and nonfailing hearts

BACKGROUND: Although cardiac sympathetic nerve dysfunction is related to poor clinical outcome, a critical sympathetic dysfunction level for predicting cardiac death is still unclear. The current study was designed to investigate which indices derived from metaiodobenzylguanidine (MIBG) imaging have prognostic value compared with clinical and cardiac function variables, and to determine the threshold of cardiac MIBG activity for identifying patients likely to suffer cardiac death in both failing and nonfailing hearts. METHODS AND RESULTS: Myocardial I-123-MIBG activity was quantified as a heart-to-mediastinum ratio in 414 consecutive patients, 173 (42%) of whom had symptomatic heart failure. After cardiac function measurements, patients were followed up with an end-point of cardiac or noncardiac death. During a mean follow-up period of 22 months, 37 cardiac deaths occurred: 23 resulted from heart failure, 9 were sudden cardiac deaths, and 5 were fatal myocardial infarctions. Multivariate analysis using the Wald chi2 and the Cox proportional hazard model revealed that late heart-to-mediastinum ratio, the use of nitrates, early heart-to-mediastinum ratio, and left ventricular ejection fraction were independent predictors of cardiac death; late heart-to-mediastinum ratio, New York Heart Association (NYHA) class, the presence of previous myocardial infarction, and age were independent predictors of heart failure and sudden cardiac death. Late heart-to-mediastinum ratio was the most powerful predictor of overall cardiac death among the variables. The Kaplan-Meier analysis showed that a late heart-to-mediastinum ratio of 1.74 or less, age greater than 60 years, the presence of myocardial infarction, and NYHA functional class 3 or 4 strongly indicated poor clinical outcomes. Furthermore, the more powerful incremental prognostic values were obtained by using MIBG imaging in combination with conventional clinical variables. CONCLUSIONS: Impaired cardiac sympathetic innervation assessed by MIBG activity has the greatest potential for predicting cardiac death and may be useful for identifying a threshold level for selecting patients at risk for death by heart failure, sudden cardiac death, and fatal myocardial infarction.     

Evaluation of transmitral flow velocity profile in supine and sitting positions by pulsed Doppler echocardiography in elderly hypertensives

To evaluate left ventricular diastolic filling properties in elderly hypertensive case with left ventricular hypertrophy (LVH), we investigated the influence of postural change from a supine to sitting position on transmitral flow velocity profile as assessed by pulsed Doppler echocardiography in 12 normotensives (N group) and 24 hypertensives, aged 65 to 80 years. Hypertensive subjects were divided into two groups on the basis of left ventricular mass index (LVMI): 12 hypertensives without LVH (H1 group; LVMI < 130 g/m2); 12 hypertensives with LVH (H2 group; LVMI > 130 g/m2). Peak early filling velocity (E), peak atrial filling velocity (A) and the E/A ratio were similar in the three groups in the supine position. The postural change decreased E and A in N and H1 groups. On the other hand, the change decreased E, but not A in the H2 group. The E/A ratio was decreased in the H2 group compared with both the N and H1 group in the sitting position. As a result, the sitting position increased atrial contribution to diastolic filling in the H2 group. These observations indicate that a reduction in preload changes the transmitral flow velocity profile in elderly hypertensives with left ventricular hypertrophy. The Doppler alterations may be related to impaired left ventricular diastolic function.     

Hypertensive cardiac hypertrophy--is genetic variance the missing link?

1. Hypertensive cardiac hypertrophy is a major independent predictor of adverse cardiovascular events. In man the cardiac response to increased afterload is very variable, even when ambulatory blood pressure monitoring is used. Analysis of breeding experiments using normotensive and hypertensive rat strains, human twin studies and other data indicate that genetic factors play a significant role in regulating cardiac mass; in other words, a large component of total variability is accounted for by genetic variance. 2. The observation that some patients with only mild-to-moderate hypertension exhibit gross left ventricular hypertrophy (LVH) similar to the inherited hypertrophic cardiomyopathies such as familial hypertrophic cardiomyopathy (FHC) and Friedreich's ataxia (FA) has prompted us to investigate the hypothesis that genetic factors associated with excessive myocardial hypertrophy, viz. mutations in FHC and FA genes alter the hypertrophic response of the heart to pressure overload. Here we review briefly three lines of study: (i) association analysis to test whether the allele frequencies differ in hypertensive patients with or without left ventricular hypertrophy; (ii) characterization of the cardiac manifestations of FA to understand the mechanism by which the heart is affected in a disease associated with pathology in a subgroup of neurons, and (iii) creation of transgenic models to facilitate the investigation of the interaction between hypertrophic stimuli and underlying genetic predisposition. 3. Information on the nature of the cardiac-mass-modifying genes involved may be useful not only for selecting high risk patients in strategies aimed at preventing the development of LVH, but also in opening new avenues of research on the reprogramming of cardiac myocytes to encourage them to hypertrophy in situations where cardiac muscle has been damaged or is hypoplastic.     

Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension

BACKGROUND: Left ventricular hypertrophy (LVH) represents an independent risk factor in patients with essential hypertension. Because reversal of LVH may be associated with an improvement of prognosis, the influence of new antihypertensive compounds, such as angiotensin II AT1 receptor antagonists, on LVH should be determined. METHODS AND RESULTS: In a randomized, double-blind trial, 69 predominantly previously untreated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m2 in men and >110 g/m2 in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Echocardiographic data of 58 patients were available. After 8 months of valsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/m2 (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/-25 to 117+/-27 g/m2 (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m2 under valsartan and only to 10 g/m2 under atenolol (R=0.91; 90% CI, 0.85 to 0.97 versus atenolol). Baseline mean blood pressure values were determined to be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/-14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatment, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsartan and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the valsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide. CONCLUSIONS: Antihypertensive treatment with the angiotensin II antagonist valsartan for 8 months produced a significant regression of LVH in predominantly previously untreated patients with essential hypertension. The drug may be safely administered in this subset of hypertensive patients; however, the long-term benefit in terms of risk reduction has still to be evaluated in further trials.     

Scintigraphic assessment of silent myocardial ischaemia after early infarction using myocardial SPET imaging with 201Tl and 123I-MIBG

To test the hypothesis that myocardial sympathetic denervation reflects silent myocardial ischaemia early after infarction, 12 patients with myocardial infarction but without post-infarction angina pectoris underwent single photon emission tomography (SPET) at rest with 201Tl and 123I-metaiodobenzylguanidine (MIBG) shortly after and 3 months after infarction. Short-axis SPET images at the basal, mid-ventricular and apical portions of the left ventricle were selected, and each short-axis image was divided into eight segments. Tracer uptake in each of the 24 segments was scored using a 4-point scale. The total score in each segment was calculated as the defect score for each image, and the difference between the total defect score for the 201Tl and 123I-MIBG images was calculated as the delta defect score. All 12 patients underwent exercise stress 201Tl scintigraphy 1 month after infarction, and they were divided into two groups: those patients with (Group A, n = 7) and those patients without (Group B, n = 5) transient perfusion defects in the peri-infarcted region without chest pain. For the 123I-MIBG defect score, a marked reduction at 3 months was observed in Group A (24 +/- 12 vs 13 +/- 6; P < 0.01), whereas the defect score remained unchanged in Group B (25 +/- 7 vs 23 +/- 8; N.S.). The delta defect score was significantly reduced in Group A (10 +/- 5 vs 6 +/- 4; P < 0.05), whereas it remained unchanged in Group B. The 123I-MIBG defect score early after infarction was higher than the exercise-induced 201Tl defect score (24 +/- 12 vs 20 +/- 9; P < 0.01), whereas at 3 months post-infarction it was lower than the exercise-induced 201Tl defect score (13 +/- 6 vs 20 +/- 9; P < 0.05). Moreover, effort chest pain during daily activities was noted in 5 of the 7 (71%) patients in Group A within 3 months post-infarction. The results of this study suggest that viable but denervated myocardium (mismatched 123I-MIBG defects) is present in peri-infarcted regions, and that myocardial sensory nervous disturbance, which may co-exist with sympathetic nervous denervation, may induce silent myocardial ischaemia in patients with myocardial infarction.     

Effects of antihypertensive therapy on left atrial function

OBJECTIVES: To investigate left atrial (LA) function as a reservoir, as a conduit and as a booster pump in essential hypertension (EH). LA volumes were echocardiographically measured in 28 untreated hypertensive patients and in 20 control subjects. BACKGROUND: LA makes a large contribution in left ventricular filling, especially in patients with impaired diastolic function. LA function is fundamental in left ventricular filling in hypertensive patients as hypertension results in left ventricular diastolic dysfunction. METHODS: Diagnosis of EH (blood pressure > 140/90 mm Hg) was based on three repeated readings of blood pressure (BP). Patients with myocardial infarction, cardiomyopathy, valvular or congenital heart disease were excluded. Doppler diastolic early (E) and late (A) velocity of mitral inflow were measured. The following indexes were calculated: left ventricular mass index (LVMI) using the Penn convention; left ventricular stroke volume (LVSV); LA reservoir volume (LARV = LA maximal volume at mitral valve opening minus minimal volume); LA conduit volume (LACV = LVSV-LARV). Atrial systolic function was assessed by calculating the active emptying fraction (volume at onset of atrial systole minus minimal volume/volume at onset of atrial systole, the E/A ratio and the LA ejection force (0.5 rho A2 MOA, where rho = the density of blood, MOA = mitral orifice area from the parasternal short axis view). Measurements were obtained in all hypertensive patients before and after 16 weeks administration of either enalapril (10 or 20 mg) or enalapril +/- chlorthalidone (20/25 mg) once a day. RESULTS: After 16 weeks of treatment, BP was reduced significantly (from 172/110 to 137/86 mm Hg, P < 0.001). LVMI decreased significantly as well (from 141 to 123 g/m2) although it was higher compared to controls (94 g/m2, P < 0.001). LARV decreased significantly (from 35.4 to 29.3 cm3, P < 0.05) while LACV increased significantly (from 43.8 to 51.3 cm3, P < 0.05), LA active emptying fraction and E/A ratio did not change. LA ejection force decreased significantly (from 20.9 to 18.1 kdynes, P < 0.05) but it was greater than controls (16.7 kdynes, P < 0.01). There was a positive relationship of LVMI to LARV (P < 0.01) in controls (r = 0.77) which held true in hypertensive patients, before (r = 0.72) and after treatment (r = 0.69). There was a negative relationship of LVMI to LACV (P < 0.01) in controls (r = -0.65), and in hypertensive patients untreated (r = -0.74) and after treatment (r = -0.72). CONCLUSIONS: Our results showed that in hypertensive patients, LA reservoir function increases and LA conduit function decreases, while LA ejection force increases. Antihypertensive treatment with enalapril and/or thiazide, induces normalisation of the LA function in parallel to left ventricular hypertrophy regression.     

Left ventricular hypertrophy and ambulatory blood pressure monitoring in chronic renal failure

BACKGROUND: Left ventricular hypertrophy (LVH) is both common and an important predictor of risk of death in end-stage renal failure (ESRF). In mild to moderate chronic renal failure (CRF), the timing of onset of LVH and the factors involved in its initial development have not been fully elucidated. The present study was undertaken to examine the prevalence and potential determinants of echocardiographically determined LVH in this connection, and to compare 24-h ambulatory blood pressure (BP) recordings with BP measured at a previous clinic visit. METHODS: From a cohort of 120 non-diabetic patients who had been attending a nephrology clinic, 118 agreed to participate in the study. Of these we selected for analysis 85 stable patients (37 male). Patients with known cardiovascular disease, those with a history of poor compliance with antihypertensive medication, and those in whom such medication had been changed in the previous 3 months were excluded. Clinic BP, 24-h ambulatory BP, echocardiography, body mass index (BMI), serum creatinine (SCr), creatinine clearance (CrCl), haemoglobin (Hb), fasting cholesterol (CHOL), triglyceride TRIGL), plasma glucose, calcium (Ca), phosphate (PO4), alkaline phosphatase (ALK PHOS), parathyroid hormone (PTH) concentrations, and 24-h urinary protein were assessed in all patients. Seventy-seven per cent were on antihypertensive medication. RESULTS: LVH was detected in 16% of patients with CrCL > 30 ml/min, and 38% of patients with CrCl < 30 ml/min. By stepwise regression analysis, ambulatory systolic BP (P < 0.0001), male gender (P < 0.0001), BMI (P < 0.0002), and Hb concentration (P < 0.002) were the only independent determinants of left ventricular (LV) mass. Nocturnal systolic BP (P < 0.02) was the main determinant of LVH in the group of patients with advanced CRF. The correlation between left ventricular mass index (LVMI) and mean 24-h ambulatory systolic BP (r = 0.52, 95% confidence interval 0.50-0.54) was statistically significantly stronger than with outpatient systolic BP (r = 0.25, 95% confidence interval 0.23-0.27). The same was true for the correlation between LVMI and mean 24-h ambulatory diastolic BP (r = 0.42, 95% confidence interval 0.40-0.44), and outpatient diastolic BP (r = 0.22, 95% confidence interval 0.20-0.24). CONCLUSIONS: Twenty-four hour ambulatory BP recording and echocardiography are required for accurate diagnosis of inadequate BP control and early LVH in patients with chronic renal impairment, independent determinants of which are hypertension, male sex, BMI, and anaemia.     

Various ways of calculating echocardiographic left ventricular mass and their relative prognostic values

OBJECTIVE: To compare the calculations of left ventricular mass according to thick-wall [American Society of Echocardiography (ASE) and Penn convention] and thin-wall (Wikstrand formula) models. METHODS: We have reexamined the data from the cross-sectional study on the general population sample of Vobarno and from a prospective longitudinal study of hypertensive patients assessing the prognostic significance of changes in left ventricular mass during a follow-up period of 10 years on average (Brescia population). RESULTS: For the Vobarno and Brescia populations, we found a close relationship between values of left ventricular mass calculated by using a thin-wall ellipsoidal model (Wikstrand formula) and those calculated using a thick-wall model with Penn convention or ASE left ventricle measurements (r = 0.99, for both the Vobarno and Brescia populations). Highest values of Penn left ventricle mass were slightly underestimated by use of the thin-wall formula. The numbers of nonfatal cardiovascular events and the relative risks, evaluated by Cox proportional hazard models for 151 patients seen at follow-up did not differ for patients with persistence of left ventricular hypertrophy (LVH), those with regression of LVH, and those with normal left ventricle mass, both at baseline and at follow-up, when these different ways of measuring left ventricle mass and partition values for LVH were used. CONCLUSIONS: The calculation of left ventricle mass according to the ASE recommendations or to the Penn convention, both of which are based on the assumption that the left ventricle can be represented by a prolate ellipsoid with both the internal and external long axes twice the short axis, produces results similar to those obtained using an alternate formula for the calculation of left ventricle mass, considering wall thickness constant around the ellipsoidal cavity. The cardiovascular risk stratification, in relation both to baseline left ventricular mass and to its change during long-term antihypertensive treatment, does not differ significantly among the results of these three different calculations.     

An evaluation of the British Army spatial disorientation sortie in U.S. Army aviation

A 68-year-old female whose myocardial sympathetic function was severely damaged with multi-vessel vasospastic angina is presented. She had no signs of autonomic dysfunction or diabetes mellitus. Myocardial imaging with 123I-MIBG showed extremely diminished uptake, but 201TlCl and 123I-BMIPP SPECT images were almost normal. Coronary arteriography revealed no significant atherosclerotic stenosis, multivessel spasm was observed by provocation test using acetylcholine. The extremely diminished uptake of 123I-MIBG was slightly increased in response to medication and the subsequent improvement of the patient's condition. Markedly decreased uptake with 123I-MIBG myocardial scintigraphy was considered to be due to multi-vessel spastic angina. We believe that this method of imaging study is useful for evaluating the healing stage of myocardial sympathetic dysfunction.     

Increased myocardial ultrasonic reflectivity is associated with extreme hypertensive left ventricular hypertrophy: a tissue characterization study in humans

We assessed myocardial reflectivity pattern in a large spectrum of left ventricular mass values, covering the extremes from absent to severe myocardial hypertensive hypertrophy. Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to the morphometrically evaluated collagen content in humans. We enrolled 88 essential hypertensives. With an echo prototype implemented in our Institute, integrated values of the radiofrequency signal of myocardial walls were obtained and normalized for those of the pericardium (Integrated Backscatter Index, IBI, %). Left ventricular mass index (LVMI) was measured by Devereux formula. There was a weak correlation between septal IBI and LVMI (r = 0.35; P < .001). On the basis of LVMI values, three groups of hypertensives were identified, with absent (Group I, n = 23; LVMI < 125 g/m2), mild to moderate (Group II, n = 44; LVMI from 125 to 174 g/m2), or severe (Group III, n = 21; LVMI > 175 g/m2) left ventricular hypertrophy. The Integrated Backscatter Index in the septum was lower in patients of Group I (IBI = 23.3% +/- 3.6%) and II (IBI = 26.5 +/- 7.6; P = NS v Group I), in comparison with patients of Group III (IBI = 31.1 +/- 5.9; P < .02 v II; P < .0001 v I). An increased myocardial wall reflectivity is detectable only in the presence of extreme forms of hypertensive left ventricular hypertrophy.     

Left ventricular geometry as an independent predictor for extracardiac target organ damage in essential hypertension

Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. It has not been established, however, whether left ventricular geometry is an independent predictor of extracardiac target organ damage in essential hypertension. Study groups were classified according to relative wall thickness: 27 patients with concentric LVH and 50 patients with eccentric LVH. Age and left ventricular mass indexes of two groups were matched. As indexes of extracardiac target organ damage, retinal funduscopic grade, and serum creatinine level were measured. The severity of hypertensive retinopathy and the renal involvement were more severe in patients with concentric LVH than in patients with eccentric LVH. Extracardiac target organ damage was consistently higher in patients with concentric LVH than in those with eccentric LVH. Systemic hemodynamics paralleled ventricular geometric patterns, with higher peripheral resistance and lower aortic compliance in patients with concentric LVH, whereas end-diastolic volumes and stroke volumes were higher in patients with eccentric LVH than in patients with concentric LVH. In addition, total peripheral resistance was related to retinal fundoscopic grade (r = 0.41, P < .01), and serum creatinine level (r = 0.28, P < .05). Even in the presence of an identical degree of LVH, echocardiographically determined left ventricular geometry may provide a further independent stratification of extracardiac target organ damage in essential hypertension.     

Left ventricular hypertrophy, blood pressure and ACE genotype in untreated hypertension

It has been suggested that the deletion polymorphism of the angiotensin-converting enzyme (ACE) genotype may be important in the development of left ventricular hypertrophy (LVH). In order to test this hypothesis we investigated the interaction between blood pressure (BP), LVH and ACE genotype in 86 previously untreated hypertensive patients. Each underwent two-dimensional and Doppler echocardiography and ACE genotyping. There were no significant differences in BP, the parameters of left ventricular structure (including left ventricular mass index) or diastolic function between the three genotype groups. Additionally, there were no significant differences in the relationship between systolic BP and left ventricular mass index among the three genotype groups (II genotype, r = 0.46, P = 0.02; ID genotype, r = 0.42, P = 0.01; DD genotype, r = 0.34, P = 0.10; F = 0.38). In contrast to some previous studies, we have found in this group of previously untreated hypertensive subjects no evidence to suggest that the deletion polymorphism of the ACE genotype is important in the development of LVH.