Silent myocardial ischaemia and left ventricle hypertrophy in diabetic patients

The purpose of this study was to evaluate the ability of three noninvasive techniques to detect silent myocardial ischaemia and analyse the factors associated with this condition, particularly left ventricular hypertrophy, in diabetic patients. An ECG stress test, a thallium-201 myocardial scintigraphy with dipyridamole intravenous infusion, ambulatory 48 h ECG monitoring and an echocardiographic study were performed in 92 diabetic patients without cardiac symptoms but with > or = 2 additional cardiovascular risk factors. At least one of these tests was positive in 28 patients (30.4%), suggesting silent myocardial ischaemia. Twenty-four of these patients had a coronary angiography which showed significant coronary stenosis in only 9 cases. An accurate echocardiographic tracing was obtained in 79 patients, particularly in 7 of the 9 with coronary stenosis. Left ventricular hypertrophy was detected in 34 patients, 6 of whom had coronary stenosis. In patients with left ventricular hypertrophy, the positive predictive values of myocardial scintigraphy and the ECG stress test were respectively 50% and 100%, as compared to only 33% and 11% in those without hypertrophy. In summary, coronary stenoses were found in < 10% of asymptomatic diabetic patients with > or = 2 cardiovascular risk factors, but more frequently in individuals with left ventricular hypertrophy. Thus, silent myocardial ischaemia should be searched for first in diabetic patients with hypertrophy, for which the stress test was the most accurate detection method in this study.     

Effect of 3 hypertensive++ agents on ventricular geometry and function

BACKGROUND: To assess the prevalence of left ventricular hypertrophy in hypertensive patients referred to an outpatient cardiology unit, and to assess its evolution under antihypertensive treatment. METHODS: One hundred and seven mild to moderate hypertensive patients were randomized to receive either xipamide, verapamil or atenolol. Cross-sectional echocardiography was performed in order to assess left ventricular mass and function. RESULTS: Mean age was 56 years, with a 4:1 female/male ratio. Mean follow-up was 120 days. Left ventricular hypertrophy was very common (65%) and decreased to 54% under antihypertensive treatment. Left ventricular mass decreased from 134.3 g/m2 to 118.1 g/m2 (p < 0.001). Concentric hypertrophy was the most common geometric pattern (42%), decreasing to 30% with treatment. Xipamide decreased ventricular mass by decreasing left ventricular diameters, while verapamil and atenolol decreased left ventricular thickness, mainly in septal wall. Systolic function was not modified during the treatment period. Diastolic function was not modified by xipamide and verapamil, and improved with atenolol. CONCLUSIONS: Left ventricular hypertrophy is very frequent when determined by echocardiography and all three drugs produced regression of left ventricular hypertrophy in a different way with respect to left ventricle geometry, an effect which could have potential therapeutic implications.     

Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.     

Chain elongation in the isoprenoid biosynthetic pathway

PURPOSE: To investigate the associations between specific preoperative 12-lead electrocardiogram (ECG) abnormalities, perioperative ischemia, and postoperative myocardial infarction or cardiac death in major vascular surgery. METHODS: Two prospective studies on perioperative myocardial ischemia performed in two tertiary university hospitals were combined to include 405 patients. All preoperative ECGs were analyzed according to the Sokolow-Lyon criteria for left ventricular hypertrophy by investigators who were blinded to the patients' perioperative clinical course. Perioperative myocardial ischemia was detected by continuous ECG recording, and postoperative cardiac complications included myocardial infarction and cardiac death. RESULTS: A total of 19 postoperative cardiac complications occurred (two cardiac deaths and 17 myocardial infarctions). Voltage criteria for left ventricular hypertrophy (78 patients, 19%) and ST segment depression greater than 0.5 mm (98 patients, 24.2%) on preoperative ECGs were both significantly associated with postoperative myocardial infarction or cardiac death (odds ratio, 4.2 and 4.7; p = 0.001 and 0.0005, respectively) and with longer intraoperative and postoperative myocardial ischemia. In each of the two study groups, a preoperative ECG abnormality that involved voltage criteria, ST segment depression, or both (134 patients, 33.1%) was more predictive of postoperative cardiac complications than any other preoperative clinical variable, including a history of myocardial infarction or angina pectoris, diabetes mellitus, pathologic Q-wave by ECG, or preoperative myocardial ischemia. The combined duration of intraoperative and postoperative ischemia and the preoperative ECG with either voltage criteria or ST segment depression were the only independent factors associated with adverse cardiac events by multivariate analysis (p < or = 0.0001 and p = 0.02, respectively). CONCLUSION: Left ventricular hypertrophy and ST segment depression on preoperative 12-lead ECGs are important markers of increased risk for myocardial infarction or cardiac death after major vascular surgery.     

Magnetocardiographic QT interval dispersion in postmyocardial infarction patients with sustained ventricular tachycardia: validation of automated QT measurements

QT dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum-minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QTapex dispersions were 127 +/- 26 versus 83 +/- 21 ms (P = 0.004) and QTend dispersions 130 +/- 37 versus 82 +/- 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QTapex and 27% for QTend dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.     

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.     

Important metabolites to measure in pharmacodynamic studies of chlorpromazine

Left ventricular hypertrophy occurs in numerous hypertensive patients. It can be diagnosed by using echocardiography, whose sensibility (93%) and sensitivity (95%) are both excellent, provided the quality of the recordings is good enough (80%). Most often, left ventricular hypertrophy is a concentric one (relative wall thickness greater than 0.45). The determinants of hypertensive left ventricular hypertrophy are of mechanical and hormonal origin; Weber's and Brilla's recent findings suggest that the haemodynamic burden should be responsible for myocytes hypertrophy, whereas hormonal factors stimulate fibrosis proliferation. Although left ventricular hypertrophy is initially an adaptative process, it eventually results in numerous deleterious effects: arrhythmias, myocardial ischemia, left ventricular filling abnormalities. Left ventricular hypertrophy is now recognized as a powerful blood-pressure independent risk factor for cardio-vascular morbidity and mortality. Therefore, antihypertensive therapy must be aimed at reducing not only blood pressure but also left ventricular mass. Most of the published regression studies have however to be criticized from a methodologic standpoint.     

Value of signal-averaged electrocardiography, radionuclide ventriculography, Holter monitoring and clinical variables for prediction of arrhythmic events in survivors of acute myocardial infarction in the thrombolytic era

OBJECTIVES: This study assessed the ability of signal-averaged electrocardiography, radionuclide ventriculography and Holter electrocardiographic (ECG) monitoring and clinical variables to identify patients at risk of serious arrhythmic events after myocardial infarction in the thrombolytic era. BACKGROUND: Most studies of signal-averaged electrocardiography, radionuclide ventriculography and Holter ECG monitoring in risk stratification after myocardial infarction preceded the introduction of thrombolytic therapy. METHODS: A consecutive series of 301 survivors of myocardial infarction, 205 (68%) of whom received thrombolytic agents, underwent signal-averaged electrocardiography (1st 48 h, day 6 and discharge), Holter ECG monitoring (days 6 to 7) and radionuclide left ventriculography (days 7 to 14). Median follow-up time was 1.03 years. RESULTS: Thirteen patients (4.3%) had an arrhythmic event (sudden death in 11, sustained ventricular tachyarrhythmia in 2). The 25-Hz high pass filtered signal-averaged ECG at discharge was 64% sensitive (95% confidence intervals [CI] 36% to 92%) and 81% specific (95% CI 76% to 86%). High grade ventricular ectopic activity on the Holter ECG was only 38% sensitive (95% CI 12% to 64%) and 74% specific (95% CI 71% to 77%). Left ventricular ejection fraction < 0.4 was the best test for prediction of arrhythmic events (sensitivity 75% [95% CI 50% to 100%] and specificity 81% [95% CI 76% to 85%]). In multivariate analysis, in rank order, digoxin therapy at discharge, an abnormal 25-Hz signal-averaged ECG before discharge, absence of angina before index infarction and previous infarction were predictive of arrhythmic events. With digoxin therapy excluded, ejection fraction was an independent predictor. Discriminant analysis identified a high risk group (12% of the study patients) with an event rate of 26%. CONCLUSIONS: The signal-averaged ECG and left ventricular ejection fraction are each independently predictive of arrhythmic events after myocardial infarction, but the Holter ECG is not. A combination of clinical and investigative variables, including the signal-averaged ECG, best identifies patients at highest risk.     

Factors influencing reduction in blood pressure and left ventricular mass in hypertensive type-1 diabetic patients using captopril or doxazosin for 6 months

The effect of doxazosin versus captopril on blood pressure, albuminuria, and left ventricular mass was studied in 33 hypertensive type-1 diabetic patients randomized to 6 months treatment with captopril (17 patients, mean daily dose 100 mg) or doxazosin (16 patients, mean daily dose 9 mg). Casual and 24-h ambulatory blood pressure (24hBP) were reduced from 163/95 to 144/83 mm Hg and 152/86 to 145/81 mm Hg, respectively, in the captopril group, and from 160/93 to 145/86 mm Hg and 156/86 to 147/79 mm Hg in the doxazosin group (all P < .05). The achieved 24hBP on treatment was positively associated with pretreatment levels of glycosylated hemoglobin (HbA1c) and plasma atrial natriuretic peptide (r = 0.53 and 0.59, respectively, both P < .01). Albuminuria did not change significantly in either group. Left ventricular hypertrophy was present in 13 patients (7 in the captopril and 6 in the doxazosin group). Left ventricular mass was reduced by an average of 27% and 23%, respectively, in these patients (both P < .01), but did not change significantly in patients without left ventricular hypertrophy. The reduction in left ventricular mass was positively associated with the presence of baseline left ventricular hypertrophy and inversely with dietary sodium intake and achieved casual blood pressure on treatment (R2 = 0.59, P < .001). We conclude that doxazosin and captopril used for 6 months are equally effective in reducing blood pressure and left ventricular hypertrophy in hypertensive type-1 diabetic patients; the antihypertensive effect is closely related to glycemic control; and dietary sodium intake and achieved casual blood pressure after treatment are independent determinants of the reduction in left ventricular mass seen in these patients.     

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.     

Sudden death as a presenting symptom of hypertrophic cardiomyopathy: treatment with an implantable cardioverter defibrillator

Aborted sudden death as the presenting manifestation of hypertrophic cardiomyopathy in a 14-year-old child is reported. Documented ventricular fibrillation was the cause of cardiac arrest. No ventricular arrhythmia was induced during programmed electrical stimulation. An implantable cardioverter-defibrillator was indicated. As the patient had a family history of myocardial disease, he had undergone a cardiovascular evaluation 4 years before the major event, and was found normal. It is suggested that normal physical examination, ECG, echocardiogram should not rule out the diagnosis of hypertrophic cardiomyopathy when a family history is present. Left ventricular hypertrophy may develop during childhood in patients with hypertrophic cardiomyopathy.     

Left ventricular hypercontractility and ST segment depression in patients with syndrome X

OBJECTIVES: This study was designed to assess the relation between rest left ventricular function and exercise capacity in patients with syndrome X. BACKGROUND: Clinical observation has suggested that some patients with syndrome X have a high rest left ventricular ejection fraction. In this study we determined the relation between left ventricular ejection fraction and exercise capacity and the electrocardiographic (ECG) changes that develop on exercise. METHODS: The pattern of left ventricular function, exercise capacity and 24-h ambulatory ECG monitoring were studied in 37 patients (9 men, 28 women; mean age 52 +/- 7 years) with syndrome X (angina with normal coronary arteries and a positive exercise test result). All patients had normal findings on echocardiogram and rest ECG. All treatment was discontinued for > or = 48 h. Left ventricular ejection fraction was determined by computerized analysis of the left ventricular angiogram. In patients with syndrome X, exercise duration and heart rate were measured at 1-mm ST segment depression and at peak exercise. RESULTS: Left ventricular hypercontractility (ejection fraction > or = 80%) was observed in 12 patients (32%) (group 1), whereas 25 patients (68%) had normal left ventricular contraction (group 2). The time to 1-mm ST depression on exercise testing was significantly earlier in group 1 than in group 2 (5.13 +/- 1.03 vs. 10.76 +/- 0.63 min, respectively, p < 0.001). The magnitude of the ST segment depression at peak exercise was significantly greater in group 1 than in group 2 (2.03 +/- 0.2 vs. 1.33 +/- 0.05 mm, respectively, p < 0.001). The mean time for ST segment depression to normalize was significantly greater in group 1 than in group 2 (4.76 +/- 0.78 vs. 3.16 +/- 0.39 min, respectively, p < 0.05). Linear regression analysis of all patients with syndrome X showed a significant correlation between exercise duration and ejection fraction (r = 0.55, p < 0.001). The mean circadian variation of heart rate and episodes of ST segment depression on 24-h ambulatory ECG monitoring were similar in the two groups of patients. CONCLUSIONS: These findings indicate that approximately one third of patients with chest pain, normal coronary angiograms and a positive exercise test have left ventricular hypercontractility, and this is associated with the development of ST segment depression at a lower heart rate and work load and a longer time to normalization of ST segment depression after exercise.     

Glucose intolerance exaggerates left ventricular hypertrophy and dysfunction in essential hypertension

The influence of glucose intolerance, the preclinical stage of diabetes mellitus, on the progression of left ventricular hypertrophy and left ventricular dysfunction in essential hypertension, was assessed with two-dimensional M-mode echocardiography in age- and sex-matched essential hypertensive patients with (n = 28) or without (n = 44) glucose intolerance, and normotensive control subjects (n = 29). Left ventricular mass index in hypertensive patients with glucose intolerance was significantly higher than that in hypertensive patients without glucose intolerance (mean +/- SD, 115.6 +/- 28.2 v 102.1 +/- 22.1 g/m2; P < .05). Left ventricular diastolic function as reflected by peak lengthening rate was reduced in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.68 +/- 0.71 v 3.16 +/- 0.82/sec; P < .05). End-systolic wall stress/left ventricular end-systolic volume index, an index of left ventricular contractility, was reduced more in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.75 +/- 0.55 v 3.13 +/- 0.55 10(3) dyn.m2/cm2.mL-1; P < .01). These findings suggest that glucose intolerance accelerates progression of left ventricular hypertrophy and deteriorates left ventricular diastolic function and contractility in essential hypertension.     

Normalization of cardiac structure and function after regression of cardiac hypertrophy

Previous studies have shown regression of left ventricular hypertrophy after pharmacologic treatment of hypertensive patients; however, the impact of regression of left ventricular hypertrophy on systolic function and on left and right ventricular diastolic function remains controversial and is difficult to assess because previous studies have not included concurrently studied age-matched control groups. Left ventricular mass, systolic function, and left and right ventricular diastolic function were assessed in 27 hypertensive patients, aged 43 +/- 6 years, by echocardiographic and Doppler studies before and 1, 3, 5, and 7 months after treatment. Left ventricular mass and ventricular function were concurrently evaluated in 27 age-matched normotensive subjects. Treatment with antihypertensive agents resulted in a significant (p < 0.001) reduction in diastolic blood pressure of 15 mmHg, measured at 1 month and sustained throughout the study. In response to hemodynamic unloading, left ventricular mass index decreased from 129 +/- 30 gm/m2 at baseline to 105 +/- 26 (p < 0.05) and 88 +/- 14 gm/m2 (p < 0.05) at 1 and 3 months of treatment, respectively, and remained unchanged over the subsequent 4 months. After 3 months of treatment, left ventricular mass index was similar in treated hypertensive and control subjects. Systolic function, assessed in terms of the relationship between shortening fraction and end-systolic wall stress, was unchanged throughout the treatment period and was no different from that in control subjects. However, patients with an initially depressed shortening fraction experienced a greater increase in shortening fraction during treatment compared to those with an initially normal shortening fraction (11% +/- 4% vs 5% +/- 5%, p < 0.01) and showed an improvement in the relationship between shortening fraction and end-systolic wall stress during treatment. Ventricular filling dynamics improved during the first 3 months of treatment, after which they were unchanged. Ventricular filling dynamics were similar in treated hypertensive patients and control subjects. In conclusion, sustained hemodynamic unloading of the left ventricle results in normalization of left ventricular mass, systolic function, and left and right ventricular diastolic filling dynamics, compared to those in age-matched control subjects.     

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.     

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.     

Correlation between left ventricular hypertrophy and GAA trinucleotide repeat length in Friedreich's ataxia

BACKGROUND: Friedreich's ataxia (FA), the most common inherited ataxia, is associated frequently with cardiac hypertrophy, and death is often cardiac related. Recently, the disease has been associated with a mutation that consists of an unstable expansion of GAA repeats in the first intron of the gene encoding frataxin on chromosome 9. METHODS AND RESULTS: We studied 44 consecutive patients with FA, determined the size of GAA expansions in the frataxin gene, and examined the relation between the genotype and cardiac phenotype assessed by M-mode and two-dimensional echocardiography. All the patients were homozygous for the mutation. The size of the GAA expansion on the smaller allele varied from 270 to 1200. We found a correlation between the size of GAA expansion and the left ventricular wall thickness (r = .51, P < .001) and the left ventricular mass index (r = .45, P = .002). Left ventricular hypertrophy was observed in 81% of patients with a number of GAA repeats above the median value of 770 compared with only 14% in the other group (P = .002). CONCLUSIONS: These data demonstrate that in FA, the severity of left ventricular hypertrophy is related to the number of GAA repeats. These results suggest that abnormalities of the gene encoding frataxin, a protein of unknown function highly expressed in the normal heart, may play an important role in the modulation of cardiac hypertrophy.     

Characterization of a nontumorigenic human breast epithelial cell line stably transfected with the human estrogen receptor (ER) cDNA

The accuracy of multichannel magnetocardiography (MCG) for the non-invasive localization of cardiac arrhythmias was investigated. A non-magnetic catheter was used in phantom studies and for cardiac pacing of 6 patients. In a clinical setting, 32 patients with WPW-syndrome, 37 patients with premature ventricular complexes and 12 patients with ventricular tachycardia were studied and the MCG results compared to reference methods, including invasive electrophysiological mapping. Phantom and pacing studies demonstrated the spatial localization accuracy to be better than 15 mm for a dipole-to-dewar distance below 15 cm. In all patients with structural cardiac disease, the ectopic focus was localized at the margin of the damaged area, serving as a proof of MCG localization. Invasive mapping confirmed the MCG result whenever performed (42 patients). In 11 patients (9 WPW, 2 VT) the MCG localization result was verified by successful HF catheter ablation as a gold standard. MCG permits the non-invasive localization of cardiac arrhythmias with high spatial accuracy. MCG guided HF catheter ablation constitutes a new concept of non-invasive localization and minimally invasive causal therapy.     

Incidental high blood pressure in family practice: due to hypertension and/or left ventricular hypertrophy in more than half of the patients

OBJECTIVE: To determine if patients with incidentally high blood pressure actually have hypertension and if these patients have an increased left ventricular mass. DESIGN: Cross-sectional study. SETTING: Two family practices with 8 general practitioners in Leiden and Noordwijk, the Netherlands. METHODS: From the Family Practice Network in the Leiden area 133 (67%) out of 200 patients with incidental high blood pressure, who did not receive antihypertensive medication, participated in the study. Their blood pressure was measured 6 times with a mercury manometer, an automatic, non-invasive ambulatory blood pressure monitoring during 24 hours was performed once and their left ventricular mass was measured by means of echocardiography. RESULTS: Of the 133 selected patients 46% had a mean diastolic blood pressure > 95 mmHg measured with the mercury manometer and 64% had a mean 24-hr diastolic blood pressure > 90 mmHg measured with the ambulatory blood pressure monitor. The correlation between both blood pressure measurements was moderate (correlation coefficient 0.73). Left ventricular hypertrophy was found in 53% of the patients, irrespective of their blood pressures. CONCLUSION: In this investigation 45-65% of patients with an incidentally high blood pressure had a mean diastolic pressure > 95 mmHg as measured with a mercury manometer and (or) a mean 24-hr diastolic blood pressure > 90 mmHg as measured with the ambulatory blood pressure monitor; 53% had left ventricular hypertrophy.     

An evaluation of the cardioprotective action of the preparation ICRF-187 (Cardioxane) during the treatment of breast cancer with large doses of adriamycin

Twenty females with disseminated breast cancer received courses of polychemotherapy with 21-day intervals. The regimen comprised adriamycin (ADM), cyclophosphamide and 5-fluorouracil in the dose 50, 500 mg/m2, respectively. 30 minutes prior to the treatment the patients were given the cardioprotector cardioxan (1000 mg/m2). Cardiological control (ECG, EF according to echo-CG and radionuclide ventriculography, PP/EP M1/M2, T1/T2 according to echo-polycardiography and Doppler cardiography) was performed before the treatment and at ADM total dose 200-300 mg/m2 followed by measurements at each dose increase by 100 mg/m2. The findings showed no evidence of ADM-related cardiac damage up to ADM dose 900-1000 mg/m2 in the case of cardioxan protection, though there was a tendency to M1/M2 increase which needs further studies as it suggests worsening of left ventricular diastolic contractility.