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Background Clinical risk factors associated with heart failure (HF) symptoms in aortic stenosis (AS) patients with preserved ejection fraction (EF) have not been fully identified. We hypothesized that left ventricular (LV) diastolic stiffness is associated with HF symptoms in patients with AS. Methods and Results We retrospectively evaluated 275 patients with at least moderate AS (aortic valve area 2 ) and preserved EF (≥50%). LV diastolic stiffness was evaluated with the use of echocardiographic parameters, diastolic wall strain (DWS, a measure of LV wall stiffness), and K LV (a marker of LV chamber stiffness). There were 69 patients with HF. Patients with HF were older, were more likely to be African American, had a higher body mass index, and had more hypertension and coronary artery disease ( P P LV 0.17 ± 0.11 vs 0.13 ± 0.08 [ P Conclusions LV diastolic stiffness is independently associated with HF in AS patients with preserved EF.

Background— African Americans develop chronic kidney disease and pulmonary hypertension (PH) at disproportionately high rates. Little is known whether PH heightens the risk of heart failure (HF) admission or mortality among chronic kidney disease patients, including patients with non–end-stage renal disease. Methods and Results— We analyzed African Americans participants with chronic kidney disease (estimated glomerular filtration rate 2 or urine albumin/creatinine >30 mg/g) and available echocardiogram-derived pulmonary artery systolic pressure (PASP) from the Jackson Heart Study (N=408). We used Cox models to assess whether PH (PASP>35 mm Hg) was associated with higher rates of HF hospitalization and mortality. In a secondary, cross-sectional analysis, we examined the relationship between cystatin C (a marker of renal function) and PASP and potential mediators, including BNP (B-type natriuretic peptide) and endothelin-1. In our cohort, the mean age was 63±13 years, 70% were female, 78% had hypertension, and 22% had PH. Eighty-five percent of the participants had an estimated glomerular filtration rate >30 mL/min per 1.73 m 2 . During follow-up, 13% were hospitalized for HF and 27% died. After adjusting for potential confounders, including BNP, PH was found to be associated with HF hospitalization (hazard ratio, 2.37; 95% confidence interval, 1.15–4.86) and the combined outcome of HF hospitalization or mortality (hazard ratio, 1.84; confidence interval, 1.09–3.10). Log cystatin C was directly associated with PASP (adjusted β =2.5 [95% confidence interval, 0.8–4.1] per standard deviation change in cystatin C). Mediation analysis showed that BNP and endothelin-1 explained 56% and 40%, respectively, of the indirect effects between cystatin C and PASP. Conclusions— Among African Americans with chronic kidney disease, PH, which is likely pulmonary venous hypertension, was associated with a higher risk of HF admission and mortality.

Background Though left ventricular mass ( LVM ) predicts cardiovascular events ( CVD ) and mortality in African Americans, limited data exists on factors contributing to change in LVM and its prognostic significance. We hypothesized that baseline blood pressure ( BP ) and body mass index ( BMI ) and change in these variables over time are associated with longitudinal increases in LVM and that such increase is associated with greater incidence of CVD . Methods and Results We investigated the clinical correlates of change in standardized logarithmically transformed‐ LVM indexed to height2.7 (log‐ LVMI ) and its association with incident CVD in 606 African Americans (mean age 58±6 years, 66% women) who attended serial examinations 8 years apart. Log‐ LVMI and clinical covariates were standardized within sex to obtain z scores for both visits. Standardized log‐ LVMI was modeled using linear regression (correlates of change in standardized log‐ LVMI ) and Cox proportional hazards regression (incidence of CVD [defined as coronary heart disease, stroke, heart failure and intermittent claudication]). Baseline clinical correlates (standardized log‐ LVM , BMI , systolic BP ) and change in systolic BP over time were significantly associated with 8‐year change in standardized log‐ LVMI . In prospective analysis, change in standardized LVM was significantly (P=0.0011) associated with incident CVD (hazards ratio per unit standard deviation change log‐ LVMI 1.51, 95% CI 1.18 to 1.93). Conclusions In our community‐based sample of African Americans, baseline BMI and BP , and change in BP on follow‐up were key determinants of increase in standardized log‐ LVMI , which in turn carried an adverse prognosis, underscoring the need for greater control of BP and weight in this group.

Although recent data suggest that the mitral diastolic early-to-late (E/A) ratio may be prognostic in selected population-based cohorts, its predictive value for morbidity and mortality in African Americans has not yet been well studied.The study population consisted of African American participants from the Jackson cohort of the Atherosclerotic Risks in Community Study. Three subgroups of E/A ratios were defined: E/A0.7, E/A 0.7-1.5, and E/A1.5, using the middle group as reference. Cox proportional hazard models were used to assess the association between the E/A ratio and both all-cause mortality and incident cardiovascular disease (CVD). The mean follow-up period was 6.8 +/- 1.3 years.Of the 2211 participants in the study population (mean age 62 years, 65.1% women), 8.2% had an E/A ratio0.7, 84.7% had an E/A 0.7-1.5, and 7.1% had an E/A1.5. An E/A1.5 was independently associated with all-cause mortality (hazard ratio [HR] 2.18, 95% confidence interval [CI] 1.20-4.03) in the multivariable model. An E/A0.7 was associated with higher all-cause mortality (HR 1.79, 95% CI 1.17-2.73) and incident CVD (HR 1.91, 95% CI 1.29-2.83) compared with a normal E/A in the age and sex adjusted model but was not independently predictive in the multivariable model (P.05).In a population-based cohort of middle-aged African Americans, an E/A1.5 independently predicts all-cause mortality. An E/A1.5 and an E/A0.7 were both associated with incident CVD when adjusted for age and sex alone but were not independently predictive in the multivariable analysis.

Valvular heart diseases are not usually regarded as a major public-health problem. Our aim was to assess their prevalence and effect on overall survival in the general population.We pooled population-based studies to obtain data for 11 911 randomly selected adults from the general population who had been assessed prospectively with echocardiography. We also analysed data from a community study of 16 501 adults who had been assessed by clinically indicated echocardiography.In the general population group, moderate or severe valve disease was identified in 615 adults. There was no difference in the frequency of such diseases between men and women (p=0.90). Prevalence increased with age, from 0.7% (95% CI 0.5-1.0) in 18-44 year olds to 13.3% (11.7-15.0) in the 75 years and older group (p0.0001). The national prevalence of valve disease, corrected for age and sex distribution from the US 2000 population, is 2.5% (2.2-2.7). In the community group, valve disease was diagnosed in 1505 (1.8% adjusted) adults and frequency increased considerably with age, from 0.3% (0.2-0.3) of the 18-44 year olds to 11.7% (11.0-12.5) of those aged 75 years and older, but was diagnosed less often in women than in men (odds ratio 0.90, 0.81-1.01; p=0.07). The adjusted mortality risk ratio associated with valve disease was 1.36 (1.15-1.62; p=0.0005) in the population and 1.75 (1.61-1.90; p0.0001) in the community.Moderate or severe valvular diseases are notably common in this population and increase with age. In the community, women are less often diagnosed than are men, which could indicate an important imbalance in view of the associated lower survival. Valve diseases thus represent an important public-health problem.

The genesis of the J wave during hypothermia has been attributed to injury current, delayed ventricular depolarization and early repolarization, tissue anoxia, and acidosis. To our knowledge, no studies have addressed the appearance of the J wave in relation to the myocardial K+ transfer and metabolism during hypothermia. Dogs (n = 9) were progressively cooled, blood samples were taken from the aorta and coronary sinus, and myocardial tissue samples were obtained for adenosine triphosphate (ATP), creatine phosphate (CP), and glycolytic intermediate determination. In every instance, the appearance of the J wave was preceded by a net loss of K+ from the myocardium. In one dog, there was no myocardial K+ loss and the J wave was absent. The J wave appeared when the esophageal temperature was between 27° and 24°C (26.6 ± 0.73°C). At that temperature, the animals were hypotensive and bradycardic, but arterial oxygen partial pressure, carbon dioxide partial pressure, and pH were within the physiologic range at that temperature. The myocardial ATP and CP from the hypothermic dogs was lower compared with the value obtained from dogs at 37°C (p < .025 and p < .005, respectively). The levels of the glycolytic intermediates, fructose-1,6-diphosphate, dihydroxyacetone phosphate, and pyruvate, were lower and the level of lactate was higher compared with those from the normothermic dogs (not significant; p < .007, p < .02, p < .001, respectively). These findings suggest that the appearance of the J wave on electrocardiography during cooling is a result of depression of the metabolic process concerned with maintenance of the partition of ions across the cell membrane, as evidenced by decreased myocardial energy content and K+ loss during the hypothermic state.

Background— The metabolic syndrome has been associated with cardiovascular disease, but few studies have examined its relationship with subclinical measures such as echocardiographic left ventricular (LV) mass. This relationship is likely to be of particular importance in blacks, in whom both the metabolic syndrome and LV hypertrophy are common. Methods and Results— Echocardiography, performed at 1 of 4 sites in the Atherosclerosis Risk in Communities (ARIC) Study, was used to assess LV dimensions in 1572 black women and men aged 49 to 75 years in 1993–1996. Participants were categorized by number of metabolic syndrome characteristics (hypertension, dyslipidemia [low HDL cholesterol or high triglycerides], and glucose intolerance). Age-adjusted mean LV mass indexed by height (g/m) increased in a stepwise gradient with increasing number of metabolic syndrome disorders (none, any 1, any 2, all 3) in both women and men (125.1, 143.9, 153.7, 169.3 and 130.5, 148.7, 160.8, 170.2, respectively; P Conclusions— In this cross-sectional population-based study of black women and men, the degree of metabolic syndrome clustering was strongly related to LV mass and its wall thickness components. These associations are consistent with a possible influence of underlying factors such as insulin resistance or other vascular processes on myocardial thickening and not on chamber size.

Background and Purpose— Previous studies have demonstrated that echocardiographic left ventricular mass (LVM) is an independent risk factor for stroke in whites. Despite the greater burden of stroke, the echocardiographic predictors of stroke in African Americans remain poorly understood. Methods— This investigation is a retrospective analysis of prospectively collected data from the Jackson, Miss (all African American), cohort of the Atherosclerotic Risk in the Communities study. Between 1993 and 1995, 2445 participants received an echocardiogram, and a random subset (n=778) received cerebral MRI evaluating presence of infarcts or white matter disease (WMD; >3 on a scale of 0 to 9). Compared with the entire Jackson cohort, the random subset was older, had a lower body mass index (BMI), and a higher systolic blood pressure (SBP). Logistic regression models examined the relations of LVM indexed by height (LVM/height) to MRI findings adjusted for age, gender, BMI, SBP, hypertensive medications, diabetes, total/high-density lipoprotein cholesterol, smoking status, and history of myocardial infarction. Results— The 667 participants (63% women; 62±4 years of age) had a high prevalence of hypertension (68%), obesity (46%), echocardiographic left ventricular hypertrophy (49%), MRI stroke (n=133), and WMD (n=92). Adjusted LVM/height was significantly associated with prevalent MRI stroke (odds ratio [OR], 1.3; 95% CI, 1.1 to 1.7; P =0.02) and WMD (OR, 1.5; 95% CI, 1.1 to 1.9; P =0.006; OR expressed per 1 SD LVM/height, 45 g/m). Conclusion— In this randomized subset of a population-based cohort of African American adults, LVM/height was related to MRI evidence of prevalent cerebrovascular disease. The current study supports the hypothesis that LVM/height is an important risk factor for stroke in multiple ethnicities.

The distribution of echocardiographic left ventricular (LV) mass differs among ethnicities. Because ethnic-specific echocardiographic criteria for LV hypertrophy (LVH) are not established, we determined whether threshold values derived from overwhelmingly white populations are appropriate for blacks, a subgroup having more LVH. Between 1992 and 1994, LV mass was measured echocardiographically in the Jackson, Mississippi, black cohort of the Atherosclerosis Risk in Communities study. Participants free of prevalent cardiovascular disease (CVD) (n=1616; mean±SD, age 59±5.7; 65% women and 57% with hypertension) were included. The optimal LVH threshold value was selected from the continuum of LV mass index (LVMI=LV mass/height 2.7 ) using 3 methods: (1) the best operating point from the area under the resulting receiver-operating characteristic (ROC) curve predicting incident CVD; (2) the value with the smallest probability value associated with incident CVD; and (3) visual inspection of functions of LVMI and CVD in the general additive model (GAM) plot. At a median follow-up of 6.8 years, there were 192 events (coronary heart disease=87, stroke=62, and congestive heart failure=43; incidence=17.6/1000 person-years). The best operating point from the resulting ROC analysis was 51.2 g/m 2.7 for sensitivity (53.4%) and specificity (61.5%). The Cox and GAM models adjusted for age, gender, systolic blood pressure, hypertension, diabetes, smoking, total cholesterol-to-high-density lipoprotein ratio, LVH by ECG criterion, and socioeconomic status found 50 to 51 g/m 2.7 as the optimal threshold for LVH in middle-aged blacks, corresponding to a minimum probability value and to a log-hazard ratio of zero, respectively. Because these values are close to the 51 g/m 2.7 established from predominantly white populations, this cutpoint is appropriate for both groups.

Characterization of target organ damage from hypertension is of particular interest in African-Americans, and evidence from electrocardiographic studies suggests that left ventricular hypertrophy is a frequent clinical finding of considerable prognostic importance. Echocardiographic studies may permit more precise characterization of the pathologic impact of hypertension on cardiac structure and function. The objective of this study is to characterize left ventricular (LV) structure including measures of wall thickness, septal thickness, internal dimension, and mass in a middle-aged sample of African-Americans using echocardiography. This study is a cohort (cross-sectional) study in which 2445 middle-aged African-American study participants from a population-based sample initially enrolled by the Atherosclerosis Risk in Communities, Jackson, Mississippi Examination Center in 1987–1989 underwent an M-mode echocardiograpic examination at their third or fourth clinic visit in 1993–1996. Measures of LV mass, even where indexed by size were conspicuously greater in men compared to women, and men exhibited a demonstrably steeper gradient of LV mass across the rather restricted age range of the study. However, when gender specific thresholds for LV hypertrophy were utilized, African-American men appear to have lower prevalence of LV hypertrophy than women. The lowest prevalence of LV hypertrophy was observed in African-American men who did not have hypertension (28.4%). The findings confirm previous suggestions from electrocardiographic investigations that cardiac hypertrophy is common, if not epidemic in middle-aged African-American men and women, whether or not they have hypertension. (ECHOCARDIOGRAPHY, Volume 20, February 2003)

Literature remains scarce on the impact of antiretroviral medications on hypertension in the HIV population. We used the South Carolina Medicaid database linked with the enhanced HIV/AIDS system surveillance database for 1994-2011 to evaluate incident hypertension and the impact of combination antiretroviral therapy (cART) in HIV/AIDS population compared with a propensity- matched non-HIV control group. Multivariable, time-dependent survival analysis suggested no significant difference in incidence of hypertension between the HIV group and the non-HIV control group. However, subgroup analysis suggested that among the HIV-infected group, months of exposure to both non-nucleoside reverse transcriptase inhibitors (adjusted hazard ratio, 1.52; 95% confidence interval, 1.3-1.75) and protease inhibitors (adjusted hazard ratio, 1.26; 95% confidence interval, 1.11-1.44) were associated with an increased risk of incident hypertension after adjusting for traditional demographic and metabolic risk factors. In people with HIV/AIDS, prolonged exposure to both protease inhibitor-based and non-nucleoside reverse transcriptase inhibitor-based cART may increase the risk of incident hypertension.

The availability of techniques such as surgical reperfusion, angioplasty, and thrombolysis for the treatment of acute myocardial infarction (AMI) has revived interest in seeking an early detectable biochemical marker diagnostic for AMI. Therefore, we investigated whether an unidentified oxidase that is released by activated neutrophils at the onset of AMI could be used as an early diagnostic assay. The conversion by plasma oxidase of 1 μM of adrenaline to 1 μM of adrenochrome represents the plasma oxidase activity (POA) of 1 U/L. Fifty patients suspected of having AMI, 40% of whose electrocardiograms were nondiagnostic for AMI, were admitted to the coronary care unit, and venous blood samples were obtained for determination of the POA and creatine phosphokinase-MB levels. Healthy volunteers (n = 12) served as control subjects, and 8 patients with pneumonia whose leukocyte counts were greater than 15,000 μL were included in the study. In those with AMI (n = 22), as determined by serial creatine phosphokinase-MB, the mean POA (± standard error of the mean) was 233 ± 13 U/L, and in those with angina and no AMI (n = 28) was 127 ± 5 U/L (P < 0.0001). In the control group, mean POA (± standard error of the mean) was 84 ± 5 U/L (control versus angina; s 0.01) and for those with infection was 214 ± 10 U/L. At admission, the creatine phosphokinase-MB was diagnostic for only 12 of the 22 patients with AMI (sensitivity rate of 54%), whereas in 21 of those patients, the POA values were diagnostic for AMI (sensitivity rate of 95%). Determination of POA may represent an alternative sensitive method to screen for AMI or ischemia in patients with anginal symptoms and no evidence of acute infection.

A 23-year-old woman with peripartum cardiomyopathy presented with a 2.1 x 2.5-cm pedunculated, mobile, left ventricular thrombus and evidence of systemic embolization. Due to the patient's poor left ventricular function, thrombectomy was not a viable option. Treatment with high-dose IV heparin was initially utilized but was unsuccessful as the thrombus appeared to enlarge on echocardiography. An accelerated weight-adjusted dose of recombinant tissue plasminogen activator (rt-PA) successfully lysed the thrombus without evidence of embolization. Although rt-PA has been used for primary lysis of high-risk ventricular thrombi, this is the first documentation of successful lysis of a left ventricular thrombus in a patient with peripartum cardiomyopathy.

The end-systolic pressure-volume relation, the relation between stroke work and end-diastolic volume, termed the preload recruitable stroke work relation, and the relation between the peak of the first derivative of left ventricular pressure (dP/dtmax) and end-diastolic volume have been employed as linear indexes of left ventricular contractile performance in laboratory animals. The purpose of this study was to examine the relative utility of these indexes during routine cardiac catheterization in seven human subjects (mean age 48 +/- 18 [SD] years) with a normal left ventriculogram and coronary angiogram. Left ventricular pressure was recorded continuously with a micromanometer catheter, and left ventricular volume was derived from digital subtraction contrast ventriculograms obtained at 30-ms intervals. Transient occlusion of the inferior vena cava with a balloon-tipped catheter was employed to obtain beat to beat reductions in left ventricular pressure and volume over 8.7 +/- 1.7 cardiac cycles. Stroke work declined by 49 +/- 13% during vena caval occlusion, but end-systolic pressure fell by only 26 +/- 11%, and changes in dP/dtmax were small and inconsistent (12 +/- 22%). Consequently, the range of data available for determination of the preload recruitable stroke work relation greatly exceeded that for the end-systolic pressure-volume relation and the dP/dtmax-end-diastolic volume relation, and much less linear extrapolation from the measured data was required to determine the volume-axis intercept. Preload recruitable stroke work relations were highly linear (r = 0.95 +/- 0.07), and much more so than end-systolic pressure-volume relations (r = 0.79 +/- 0.23).(ABSTRACT TRUNCATED AT 250 WORDS)

Background and Purpose— The association between left atrial (LA) size, ischemic stroke, and death has not been well established in African Americans despite their disproportionately higher rates of stroke and cardiovascular mortality compared to non-Hispanic whites. Methods— For the analysis, participants in the Jackson cohort of the Atherosclerosis Risk in Communities Study were followed from the date of the echocardiogram in cycle three to the date of the first ischemic stroke event (or death) or to December 31, 2004 if no ischemic stroke event (or death) was detected. Results— There were 1886 participants in the study population (mean age 58.9 years, 65% women). Participants in the top quintile of LA diameter indexed to height (LA diameter/height; 2.57 to 3.55 cm/m) were more likely women, hypertensive, diabetic, and obese compared to those not in the top quintile. Over a median follow-up of 9.8 years for ischemic stroke and 9.9 years for all-cause mortality, there were 106 strokes and 242 deaths. In a multivariable model adjusting for traditional clinical risk factors, the top quintile of LA diameter/height was significantly related to ischemic stroke (HR 1.7; 95% CI: 1.1, 2.7) and all-cause mortality (HR 2.0; 95% CI: 1.5, 2.7). After further adjustment for left ventricular (LV) hypertrophy and low LV ejection fraction, the top quintile remained significantly related to all-cause mortality (HR 1.8; 95% CI: 1.3, 2.5). Conclusions— In this population-based cohort of African Americans, LA size was a predictor of all-cause mortality after adjusting for traditional cardiovascular risk factors, LV hypertrophy, and low LV ejection fraction.

BACKGROUND: Whether microvascular disease contributes to the development of left ventricular hypertrophy (LVH) is unclear. We examined the relationship of retinal microvascular signs with LVH in an African-American population. METHODS: A population-based, cross-sectional study of 1,439 middle-aged African-American participants in Jackson, Mississippi. A retinal photograph of one randomly selected eye was obtained and graded for presence of retinal microvascular signs (focal arteriolar narrowing, arterio-venous (AV) nicking, and retinopathy) according to standardized protocols. Retinal vessel diameter was measured from a computer-assisted technique to define generalized arteriolar narrowing. LVH was defined from standardized echocardiography. RESULTS: In age and gender-adjusted models, retinal microvascular signs (except non-diabetic retinopathy) were significantly associated with LVH, with an odds ratio (OR) of 1.64 (95% confidence interval (CI) 1.29-2.09) for generalized arteriolar narrowing, OR 1.82 (95% CI 1.33-2.50) for focal arteriolar narrowing, and OR 1.35 (95% CI 1.02-1.79) for AV nicking. With further adjustment for cardiovascular (serum total cholesterol, fasting glucose, diabetes, diabetes duration, smoking, body mass index (BMI), waist-to-hip ratio, and exercise level) and hypertension-related factors (mean arterial blood pressure (MABP) at the time of retinal photography and antihypertensive medication use), associations were attenuated but remained significant for generalized and focal arteriolar narrowing, with OR 1.35 (95% CI 1.02-1.78) and OR 1.66 (95% CI 1.16-2.38), respectively. CONCLUSIONS: Middle-aged African Americans with generalized and focal retinal arteriolar narrowing were more likely to have LVH. This association was explained only partly by cardiovascular risk factors and hypertension.

To evaluate the acute changes in left ventricular (LV) performance before and immediately after percutaneous aortic valvuloplasty, 25 patients underwent first-pass radionuclide angiocardiography for construction of pressure-volume loops. Simultaneously, high-fidelity micromanometric aortic and LV pressures were recorded. Echocardiographic wall thickness was used to define wall stress. After valvuloplasty, no acute changes were observed in the heart rate, aortic systolic pressure, cardiac output or degree of aortic insufficiency. Valvuloplasty decreased the peak aortic valve gradient from 73 to 40 mm Hg (p less than 0.001) and the mean gradient from 61 to 30 mm Hg (p less than 0.001); aortic valve area increased from 0.55 to 0.80 cm2 (p less than 0.001). Meridional end-systolic wall stress decreased from 83 to 55 X 10(3) dynes/cm2 (p less than 0.01). LV ejection fraction increased from 0.41 to 0.48 (p less than 0.01). LV end-diastolic volume decreased from 186 to 160 ml (p less than 0.001), end-systolic volume decreased from 115 to 87 ml (p less than 0.001) and end-diastolic pressure decreased from 22 to 17 mm Hg (p less than 0.01). LV stroke work decreased from 16.0 to 14.0 X 10(6) erg (p less than 0.001). No change was observed in peak positive LV dP/dt or the end-systolic pressure-volume ratio. This study documents variable and complex changes in the measures of cardiac function after aortic valvuloplasty. A decrease in the amount of LV outflow obstruction with maintenance of the cardiac output at a decreased level of LV filling occurs.

To evaluate the serial changes in right and left ventricular performance after percutaneous aortic balloon valvuloplasty, 15 patients, mean age 75 +/- 18 years, and in New York Heart Association (NYHA) class III, were studied with first-pass radionuclide angiocardiography (RNA) immediately before, then 5 minutes, 2 hours, 4 hours, 6 hours, and 3 days after valvuloplasty. No change was observed in heart rate, aortic root systolic pressure, Fick, or RNA cardiac output, amount of aortic insufficiency measured either angiographically or with the regurgitant fraction determination immediately after valvuloplasty. However, significant changes were observed in the peak-to-peak aortic valve gradient (63 to 35 mm Hg; p less than 0.001), mean aortic valve gradient (54 to 33 mm Hg; p less than 0.001), aortic valve area (0.60 to 0.90 cm2; p less than 0.001), and meridional wall stress (79 to 50 10(3) dynes/cm2; p less than 0.01) immediately following valvuloplasty. In addition, left ventricular end-diastolic volume decreased from 186 to 153 ml (p less than 0.001), end-systolic volume decreased from 114 to 86 ml (p less than 0.001), micromanometric left ventricular end-diastolic pressure decreased from 20 to 14 mm Hg (p less than 0.02), and left ventricular ejection fraction increased from 0.39 to 0.45 (p less than 0.001). Peak positive left ventricular dP/dt and end-systolic pressure-volume ratio did not change after valvuloplasty (1700 to 1550 mm Hg/sec, 2.1 to 2.5 mm Hg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Background and Purpose— Despite theories that link stroke to left ventricular mass, few large, population-based studies have examined the predictive value of echocardiographically derived left ventricular mass index (LVMI) to incident stroke in African Americans. Methods— Participants in the Jackson cohort of the Atherosclerotic Risk in Communities study have had extensive baseline evaluations, have undergone echocardiography during the third examination (1993–1995), and have been followed up for incident cardiovascular disease including ischemic stroke. Results— The study population consisted of 1792 participants, of whom 639 (35.7%) were men and the mean±SD age was 58.8±5.7 years. Compared with those without ischemic stroke, those with ischemic stroke had a higher frequency of hypertension (85.6% vs 58.7%) and diabetes (46.9% vs 21.0%). Left ventricular hypertrophy was more prevalent in those with stroke (62.2% vs 38.6%). During a median follow-up of 8.8 years, 98 incident strokes occurred (6.5 per 1000 person-years). LVMI was independently associated with stroke after adjusting for age, sex, hypertension, systolic blood pressure, smoking, diabetes, total to HDL cholesterol ratio, body mass index, and low left ventricular ejection fraction (adjusted hazard ratio per 10 g/m 2.7 increment of LVMI=1.15; 95% CI, 1.02 to 1.28). The relation remained statistically significant after adding left atrial size and mitral annular calcification to the multivariable model. Conclusions— In this large, population-based African American cohort, we found that echocardiographic LVMI was an independent predictor of incident ischemic stroke even after taking into account traditional clinical risk factors.

Published studies of the prognostic value of left ventricular (LV) hypertrophy and LV geometric pattern in African-Americans were based on referred or hospitalized patients with hypertension or coronary heart disease. All-cause mortality rates and survival associated with LV geometric pattern were determined using echocardiography in a population-based sample of middle-aged and elderly African-American men and women. During the third (1993 to 1995) visit of the ARIC Study, echocardiography was performed at the Jackson, Mississippi, field center on the cohort of 2,445 African-Americans aged 49 to 75 years. M-Mode LV echocardiographic measurements were available for 1,722 persons. Mortality data were available through December 31, 2003. During the follow-up period (median 8.8 years, maximum 10.4), 160 deaths were identified. In men, multivariable-adjusted hazard ratios for all-cause mortality (compared with men with normal LV geometry) were 1.75 (95% confidence interval [CI] 0.71 to 4.33) in those with concentric LV hypertrophy, 0.38 (95% CI 0.08 to 1.88) in those with eccentric LV hypertrophy, and 0.79 (95% CI 0.41 to 1.54) in those with concentric remodeling. In women, multivariable-adjusted hazard ratios for all-cause mortality (compared with women with normal LV geometry) were 1.17 (95% CI 0.48 to 2.84) in those with concentric LV hypertrophy, 1.23 (95% CI 0.46 to 3.28) in those with eccentric LV hypertrophy, and 1.17 (95% CI 0.60 to 2.28) in those with concentric remodeling. In conclusion, in this population-based cohort of middle-aged and elderly African-Americans free of coronary heart disease, adjustment for baseline differences in cardiovascular disease risk factors and LV mass greatly attenuated the strength of the association between LV pattern and all-cause mortality risk in women. In men, an association between concentric LV hypertrophy and mortality risk remained.

Background There are limited data on the prevalence and the clinical and echocardiographic correlates of pure valvular regurgitation in African Americans despite the higher rates of cardiovascular disease in this group. Purpose The Jackson, Mississippi, site of the Atherosclerosis Risk in Communities study provides a unique opportunity to study mitral regurgitation (MR), tricuspid regurgitation (TR), and aortic regurgitation (AR) in this population. Methods There were 2285 participants who were available for analysis. The prevalence rates of MR, TR, and AR by severity were calculated for participants aged 50 to 59, 60 to 69, and ≥70 years. Multivariable regression analyses were conducted to determine clinical and echo variables associated with the presence of MR, TR, and AR. Results Mild or greater MR and TR were present in 14.7% and 17.2% of participants, respectively. Aortic regurgitation was present in 15.6% of participants. In the multivariable regression model, MR was independently associated with age, sex, lower body mass index (BMI), systolic blood pressure, left atrial size, left ventricular (LV) diastolic diameter, and low LV ejection fraction. Tricuspid regurgitation was independently associated with age, sex, lower BMI, high-density lipid, left atrial size, and lower relative wall thickness. Aortic regurgitation was independently associated with age, sex, lower BMI, systolic blood pressure, LV diastolic diameter, LV hypertrophy, and low LV ejection fraction. Conclusion In this middle-aged African Americans cohort, the prevalence of mild to greater MR and TR was similar to that seen in other cohorts; however, AR was more prevalent. Several cardiovascular risk factors and echo parameters were identified as independent correlates of valvular regurgitation.

Background Cardiovascular risk associated with diabetes may be partially attributed to left ventricular structural abnormalities. However, the relations between left ventricular structure and diabetes have not been extensively studied in African-Americans. Methods We studied 514 male and 965 female African-Americans 51 to 70 years old, in whom echocardiographic left ventricular mass measurements were collected for the ARIC Study. In these, we investigated the independent association of diabetes with left ventricular structural abnormalities. Results Diabetes, hypertension and obesity prevalences were 22%, 57% and 45%, respectively. Unindexed left ventricular mass was higher with diabetes in both men (238.3 ± 79.4 g vs. 213.7 ± 58.6 g; p < 0.001) and women (206.4 ± 61.5 g vs. 176.9 ± 50.1 g; p < 0.001), respectively. Prevalence of height-indexed left ventricular hypertrophy was higher in women while increased relative wall thickness was similar in men and women. Those with diabetes had higher prevalences of height-indexed left ventricular hypertrophy (52% vs. 32%; p < 0.001), and of increased relative wall thickness (73% vs. 64%; p = 0.002). Gender-adjusted associations of diabetes with left ventricular hypertrophy (OR = 2.29 95%CI:1.79–2.94) were attenuated after multiple adjustments in logistic regression (OR = 1.50 95%CI:1.12–2.00). Diabetes was associated with higher left ventricle diameter (OR = 2.13 95%CI:1.28–3.53) only in men and with higher wall thickness (OR = 1.89 95%CI:1.34–2.66) only in women. Attenuations in diabetes associations were frequently seen after adjustment for obesity indices. Conclusion In African-Americans, diabetes is associated with left ventricular hypertrophy and, with different patterns of left ventricular structural abnormalities between genders. Attenuation seen in adjusted associations suggests that the higher frequency of structural abnormalities seen in diabetes may be due to factors other than hyperglycemia.

Stent fracture is uncommon but may have consequences including restenosis. To date, stent fractures reported have been related to aggressive post dilation. We describe a case that involves fracture of a stent deployed to nominal pressure. Unlike most stent fractures reported that involve stent struts only our case demonstrated circumferential disruption with complete separation of the stent segments. © 2006 Wiley-Liss, Inc.

BACKGROUND: Lymphocytic myocarditis, an immune disorder of left ventricular dysfunction with sometimes confounding clinical presentations, occurs rarely during pregnancy. CASE: At 12 weeks gestation, a multigravid patient presented with a 2-month history of nausea and vomiting. Other symptomatology included postprandial epigastric pain, loose stools, and a 10-lb (4.5-kg) weight loss. Laboratory evaluation revealed evidence of hepatic dysfunction with a coagulopathy and an absolute unconjugated hyperbilirubinemia. While undergoing evaluation, the patient deteriorated rapidly and suffered a cardiopulmonary arrest. Autopsy revealed a congested liver and spleen associated with a dilated cardiomyopathy and lymphocytic myocarditis. CONCLUSION: Medically virulent disease processes can mimic the common pregnancy complaint of nausea and vomiting. Intrinsic cardiac disease with secondary hepatic compromise is a rare cause of gastrointestinal symptomatology early in pregnancy.

To estimate prevalence of left ventricular (LV) hypertrophy and its relation to systolic function in a population-based sample of African Americans.A baseline 2D guided M-mode echocardiogram was conducted as part of a longitudinal cohort study to assess prevalence and cross-sectional relationships between echocardiographic and clinical parameters.Data were collected as part of the Atherosclerosis Risk in Communities study.Analysis is limited to 1543 African Americans, aged 51-70 years, without clinically apparent cardiovascular or echocardiographically determined valvular disease.LV hypertrophy prevalence was defined as LV mass/ height2.7or = 51 g/m2.7. LV systolic chamber function was assessed at the midwall using the ratio of observed midwall fractional shortening (MWS%) to the value predicted from circumferential end-systolic stress.The prevalence of LV hypertrophy was 33% in men, 38% in women. The prevalence of concentric hypertrophy (LV hypertrophy with relative wall thicknessor = 0.45) was greater than that of eccentric hypertrophy (men: 24% vs 9%; women: 27% vs 11% women). Observed/predicted (O/P) MWS% was strongly and inversely related to LV mass/ height2.7 (P.001) and LV hypertrophy (P.001). The O/P MWS% was inversely related to LV mass/height2.7 quartile: O/P MWS% was 106% and 99% in the first and 97% and 89% in the fourth quartile of LV mass/height2.7 for men and women, respectively. Adjusting for age, adiposity, diabetes, blood pressure, antihypertensive medication use, and smoking did not remove association between O/P MWS% and LV mass/height2.7.LV hypertrophy was highly prevalent in this population-based middle-aged sample of African Americans and was associated with poorer LV systolic chamber function.

Background Despite the potential link between mitral annular calcification (MAC) and atherosclerosis, there is limited data regarding the prevalence of MAC in African Americans and its relationship with coronary heart disease (CHD)events in this high-risk population. Methods The study population included 2409 African American participants of the Artherosclerotic Risk in Communities study (ARIC) undergoing echo examinations between 1993–1996. The primary outcome was incident CHD events [defined as fatal coronary event, hospitalized myocardial infarction or cardiac procedure]. MAC was considered a binary variable (yes/no). The Cox proportional hazard model was used for the analysis and the model was adjusted for gender, age, body mass index, hypertension, diabetes, smoking status, renal function (based on serum creatinine), high LDL and low HDL. Results Of the 2409 in the study population, 1549 (64%) were women and the mean age was 59.2 ± 5.8 years (range 49–75). MAC was positively associated with age and renal function. The overall prevalence of MAC was 4.6% for women and 5.6% for men. In participants aged ≥ 70, the prevalence of MAC was 10% in women and 15.2% in men. During a median follow-up of 4.8 years, there were 237 total incident CHD events recorded. After adjustment, the hazard ratio for CHD events among the MAC subgroup was 2.32 (95% CI, 1.11–4.87). Conclusions In this relatively young population of middle-aged African Americans, the prevalence of MAC is low; however, the presence of MAC incurs a significant risk for coronary events.

Echocardiographically determined left ventricular (LV) hypertrophy may be a stronger risk factor of cardiovascular disease (CVD) for women than for men, although it is unclear whether reported gender differences are real or attributable to confounding. We evaluated echocardiographic LV hypertrophy (defined as LV mass/height(2.7) >/=51 g/m(2.7)) collected from the African-American population of the Atherosclerosis Risk in Communities Study. Incident CVD events (57 in men, 62 in women) were determined during a median follow-up of 4.9 years (interquartile range 4.3 to 5.6) and included nonfatal myocardial infarction, cardiac death, coronary revascularization, and stroke. We conducted 2 analyses. First, we created matched samples of 340 men and 812 women who had LV hypertrophy based on propensity score and estimated the gender-specific incidence rate ratios and population-attributable risks. Second, we evaluated the complete cohort (604 men and 1,113 women) with Poisson's regression after adjusting for age, body mass index, hypertension, diabetes mellitus, ratio of total cholesterol to high-density lipoprotein cholesterol, current smoking, and education level. LV hypertrophy was significantly predictive of incident CVD, and the association shown by analyses of matched propensity scores was similar in men and women (incidence rate ratio 1.88 vs 1.92, p = 0.97 for men, population-attributable risk 0.22 vs 0.26, p

We compared the short-term hemodynamic effects of intravenous fructose 1,6-diphosphate (FDP) administration in patients with coronary artery disease. Hemodynamic measurements were performed before and after administration of FDP in two groups of patients: those with impaired left ventricular (LV) function, elevated LV end-diastolic pressures (LVEDP > or =12 mm Hg, n = 30), and those with normal LV function (LVEDP

Although impaired ventricular function has been shown to improve after aortic valve replacement, there are few data on hemodynamic changes after balloon aortic valvuloplasty based on follow-up catheterization. Of 71 patients surviving 6 months after balloon aortic valvuloplasty, 41 agreed to late recatheterization. All patients had pre- and postvalvuloplasty and 6 month catheterization data measured with high fidelity micromanometer pressure recordings and simultaneous digital subtraction left ventriculography.The hemodynamic result immediately after valvuloplasty included a reduction in the aortic valve gradient and a moderate increase in aortic valve area (0.51 ± 0.14 to 0.81 ± 0.19 cm2, p < 0.0001). Ejection fraction increased slightly (52 ± 18 to 55 ± 17%, p < 0.0001) despite a decrease in peak positive rate of rise of left ventricular pressure (dP/dt 1,650 ± 460 to 1,500 ± 490 mm Hg/s, p < 0.05). There was also a decrease in left ventricular afterload and a small decrease in preload.At 6 month recatheterization, the mean aortic valve gradient and area were similar to baseline values, with 31 (76%) of 41 patients demonstrating valvular restenosis. At 6 months many left ventricular hemodynamic variables, including peak positive dP/dt and stroke work, also resembled prevalvuloplasty values. However, left ventricular end-diastolic volume was reduced (111 ± 40 ml at 6 months versus 136 ± 52 ml before valvuloplasty, p < 0.01). The mean left ventricular ejection fraction was unchanged from prevalvuloplasty values in the study group of 41 patients, but was significantly improved in 9 of 15 patients with a baseline ejection fraction

To evaluate acute and follow-up changes in left ventricular diastolic performance, simultaneous digital left ventriculography and micromanometry were performed in 49 patients undergoing aortic balloon valvuloplasty. All patients improved symptomatically after valvuloplasty, and 26 returned 6.3 ± 1.5 months later for follow-up catheterization.Immediately after valvuloplasty, aortic valve area increased (before 0.5 ± 0.2 versus after 0.8 ± 0.2 cm2, p < 0.01), cardiac output (before 4.3 ± 1.2 versus after 4.4 ± 1.3 liters/min) and ejection fraction (before 51 ± 18% versus after 52 ± 17%) did not change and diastolic indexes worsened, signified by a decrease in peak filling rate (before 247 ± 80 versus after 226 ± 78 ml/s, p < 0.01) and increase in the time constant of isovolumetric relaxation (π) (before 78 ± 29 versus after 96 ± 40 ms, p < 0.01) and the modulus of chamber stiffness (before 0.107 ± 0.071 versus after 0.141 ± 0.083, p < 0.01).At follow-up catheterization, 16 patients continued to have symptomatic improvement (group 1) and 10 had recurrence of symptoms (group 2). Aortic valve area, cardiac output and ejection fraction at follow-up catheterization in both groups were similar and unchanged from values before valvuloplasty. However, diastolic indexes and left ventricular mass were improved compared with values before valvuloplasty in group 1 and worse in group 2 as follows: peak filling rate: group 1 ±8% versus group 2 −20%, p = 0.001; time constant of isovolumetric relaxation: group 1 −11% versus group 2 ±35%, p = 0.008; chamber stiffness: group 1 −27% versus group 2 ±26%, p = 0.001; mass: group 1 −9% versus group 2 ±6%, p = 0.004.These data indicate that 1) diastolic performance worsens immediately after valvuloplasty, consistent with the development of ischemia during balloon inflation; and 2) changes in left ventricular diastolic indexes and mass, rather than aortic valve area or systolic indexes, correlate best with symptomatic status 6 months after valvuloplasty.

Carney et al 1 recently described a complex consisting of myxomas (cardiac, cutaneous and mammary), pigmentation (cutaneous and mucucutaneous) and endocrine overactivity (Cushing syndrome, sexual precocity and acromegaly). Another such case is described herein.

The relationship between dynamic changes in aortic valve gradient and left ventricular ejection performance in the early period after successful percutaneous aortic valvuloplasty has not been described in detail. Accordingly 20 adult patients with severe symptomatic calcific aortic stenosis underwent first-pass radionuclide angiography and Doppler echocardiography before, immediately after, and 2 to 4 days after the valvuloplasty procedure. A significant (p less than 0.001) reduction in peak-to-peak (72 +/- 24 mm Hg to 36 +/- 11 mmHg) and mean (60 +/- 20 mm Hg to 34 +/- 9 mm Hg) transaortic gradient and an increase in aortic valve area (0.5 +/- 0.2 cm2 to 0.8 +/- 0.2 cm2) were measured by high-fidelity micromanometer catheters immediately after aortic valvuloplasty. Results of Doppler echocardiography showed a significant (p less than 0.001) immediate decrease in peak instantaneous (81 +/- 22 mm Hg to 53 +/- 15 mm Hg) and mean (48 +/- 14 mm Hg to 31 +/- 9 mm Hg) aortic gradients. However, 2 to 4 days later a significant (p less than 0.001) return of peak (56 +/- 15 mm Hg to 65 +/- 20 mm Hg) and mean (31 +/- 9 mm Hg to 39 +/- 12 mm Hg) transvalvular gradient occurred. Aortic valve area as determined by the continuity equation also increased from 0.4 +/- 0.2 cm2 to 0.6 +/- 0.2 cm2 immediately after the procedure (p less than 0.001), then partially returned to baseline (0.5 +/- 0.2 cm2; p less than 0.005) at 2 to 4 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Doppler mitral flow indexes and their relation to invasively measured hemodynamic diastolic indexes were assessed in 13 patients with isolated aortic stenosis (AS), and compared to Doppler indexes in 10 normal subjects matched for age, heart rate, left ventricular (LV) ejection fraction and LV load. Patients with AS showed no difference in Doppler early filling (E) indexes, but demonstrated greater Doppler atrial filling (A) indexes in comparison to normal subjects: atrial velocity (89 +/- 31 vs 56 +/- 7 cm/s), atrial integral (11.4 +/- 4.8 vs 5.7 +/- 1.6 cm), A/E velocity (1.69 +/- 0.89 vs 1.06 +/- 0.26) and A/E integral (3.53 +/- 6.64 vs 0.81 +/- 0.27) (all p less than 0.05). Doppler indexes in patients with AS did not correlate with hemodynamic indexes of LV relaxation or chamber stiffness. Significant correlations were observed between Doppler and angiographic peak filling rates (r = 0.70) and between Doppler atrial filling velocity and LV end-diastolic volume (r = -0.66), LV end-diastolic pressure (r = -0.48) and LV ejection fraction (r = 0.53) (all p less than 0.05). These data indicate that, compared to matched normal subjects, most patients with AS have an increased atrial contribution to LV filling. However, in patients with decreased LV function, atrial function may also be depressed, as indicated by a decreased atrial contribution to LV filling, resulting in "normalization" of the Doppler mitral flow pattern.

In order to validate the measurement of pressure-volume loops and stroke work in humans, simultaneous digital subtraction ventriculography (DSA) and first-pass radionuclide angiocardiography (RNA) coupled with high-fidelity micromanometer left ventricular pressure measurements were undertaken in 34 patients, mean age 75 +/- 9 years, with aortic stenosis. Twenty-nine patients had a repeat study after balloon valvuloplasty, for a total of 63 DSA and RNA pressure-volume loops. All data were analyzed in a systemic fashion in order to minimize intra- and interobserver error. Linear regression analysis was used to calculate the degree of agreement between the two technologies. Left ventricular ejection fraction (RNA: 0.47 +/- 0.17, DSA: 0.49 +/- 0.18) had a correlation coefficient of 0.96; left ventricular end-diastolic volume (RNA: 171 +/- 42 ml, DAS: 168 +/- 52 ml) and end-systolic volume (RNA: 95 +/- 50 ml, DSA: 89 +/- 50 ml) had correlation coefficients of 0.89 and 0.95, respectively. Left ventricular stroke volume (RNA: 75 +/- 26 ml, DSA: 75 +/- 27 ml) had a correlation coefficient of 0.92, while integrated pressure-volume loop or stroke work (RNA: 15.6 +/- 6.6 ergs 10(6), DSA: 15.9 +/- 6.3 ergs 10(6] had a correlation coefficient of 0.89. These data demonstrate that RNA measurements of left ventricular chamber dynamics concur with that obtained with DSA. With semiautomated data analysis, the portable first-pass RNA pressure-volume data are also less labor-intensive. Moreover, multiple measurements of ventricular performance during hemodynamic manipulations in the catheterization laboratory or operating room would allow for a more precise estimation of left ventricular performance.

Study objective To prospectively investigate the evidence for embolic phenomena associated with percutaneous mitral and aortic valvuloplasty. Design Prospective, consecutive case series before and after balloon valvuloplasty. Setting Referral center hospital and cardiac catheterization laboratory. Patients Consecutive sample of 32 patients having balloon valvuloplasty for critical symptomatic stenosis of the mitral or aortic valve. Twenty-six patients had aortic stenosis; 6 had mitral stenosis. Intervention Computed tomography of the head, funduscopy, and electrocardiography were done in all patients before and after valvuloplasty. Cardiac isoenzymes were measured serially in 19 patients. Measurements and main results Previous cerebral infarction was seen in nine patients, with three showing a new abnormality after aortic valvuloplasty. In one of these patients a funduscopic hemorrhage was detected by photography. Total creatinine kinase and MB fraction were elevated in 1 of 19 patients. Serial electrocardiograms were unchanged in all patients. Conclusions The incidence of cerebral neurologic events and myocardial injury are acceptably low after balloon valvuloplasty of calcific aortic and mitral stenosis. Both episodes of symptomatic cerebral infarction occurred in patients with apparent bicuspid aortic valvular stenosis, suggesting that calcific bicuspid aortic stenosis may be associated with more neurologic events after aortic valvuloplasty.

Cardiac disease is the most important cause of non-obstetrical maternal death. 1 Atrial septal defect (ASD), which has a 2:1 female predominance, is the most common congenital heart disease during pregnancy. 1 Echocardiographically guided cardiac catheterization may be an option in patients in whom definitive hemodynamic data are needed for decision making. 224

This study evaluated whether an exercise treadmill test could predict restenosis in 289 patients 6 months after a successful emergency angioplasty of the infarct-related artery for acute myocardial infarction. After excluding those with interim interventions (64), medical events (36), or medical contraindications to follow-up testing (25), both a treadmill test and a cardiac catheterization were completed in 144 patients, 88% of those eligible for this assessment. Four patients with left bundle branch block or pacemaker rhythm at the time of treadmill testing were also excluded from analysis. Of six follow-up clinical and treadmill variables examined by multivariable logistic regression analysis, only exercise ST deviation was independently correlated with restenosis at follow-up (chi 2 = 5, p = 0.02). The clinical diagnosis of angina at follow-up, although marginally related to restenosis when considered by itself (p = 0.04), did not add significant information once ST deviation was known. The sensitivity of ST deviation of 0.10 mV or greater for detecting restenosis was only 24% (13 of 55 patients), and the specificity was 88% (75 of 85 patients). The sensitivity of exercise-induced ST deviation for detection of restenosis was not affected by extent or severity of wall motion abnormalities at follow-up, by the timing of thrombolytic therapy or of angioplasty, or by the presence of collateral blood flow at the time of acute angiography. A second multivariable analysis evaluating the association of the same variables with number of vessels with significant coronary disease at the 6-month catheterization found an association with both exercise ST deviation (p = 0.003) and exercise duration (p = 0.04). Angina symptoms and exercise treadmill test results in this population had limited value for predicting anatomic restenosis 6 months after emergency angioplasty for acute myocardial infarction.

A clinical observation of chest pain associated with the onset of rate-related left bundle branch block has been described in patients with normal coronary arteriograms. The authors used standard cardiac rehabilitation techniques for exercise training in a 47- year-old woman with these manifestations. Serial treadmill tests revealed that during the course of 3 months of exercise training, the heart rate at onset of LBBB gradually rose from 133 to 175 beats per minute, and she no longer developed symptoms during her routine daily activities or exercises. Exercise training was a successful nonpharmacologic strategy that delayed the onset of rate-related LBBB and chest pain in this patient and avoided the need for beta blocker therapy.

Background Epidemiological and clinical studies frequently use echocardiography to measure LV wall thicknesses and chamber dimension for estimating quantitative measures of LV mass. While echocardiographic M-mode LV images have traditionally been measured using hand-held calipers and strip-chart paper tracings, digitized M-mode LV image measurements made directly on the computer screen using electronic calipers have become standard practice. We sought to determine if systematic differences in LV mass occur between the two methods by comparing LV mass measured from simultaneous M-mode strip chart recordings and digitized recordings. Methods The Atherosclerosis Risk in Communities study applied the latter method. To determine if systematic differences in LV mass occur between the two methods, LV mass was measured from simultaneous M-mode strip chart recordings and digitized recordings. Results We found no difference in LV mass (p > .25) and a strong correlation in LV mass between the two methods (r = 0.97). Neither age, sex, nor hypertension status affected the correlation of LV mass between the two methods. Conclusions We conclude that digital estimates of LV mass provide unbiased estimates comparable to the strip-chart method.

Study objective To determine the incidence of cardiovascular and renal toxicity of a nonionic contrast agent when used for cardiac catheterization, and to assess the value of electrolytes and urinalysis results as predictors of nephropathy induced by a contrast agent. Study design Nonrandomized trial using a criterion standard and a cohort analytic study with a 48-hour follow-up. Setting Referral-based university hospital. Patients Convenience sample of patients having diagnostic cardiac catheterization. Renal function and clinical status were evaluated at baseline in 1,144 patients; at 24 hours in 1,077 (94%); and at 48 hours in 663 (57%). Interventions After patients received saline for hydration, coronary angiography and left ventriculography were done with iopamidol (average dose, 203 +/- 56 cc). Measurements and main results The definite and possible incidence of major acute cardiovascular complications from nonionic contrast media was 0.2% and 0.7%, respectively. The mean serum creatinine level increased 11.5 mumol/L from baseline at 24 hours (P less than 0.0001) and 16.8 mumol/L from baseline at 48 hours (P less than 0.0001). Results in a randomly selected training sample were studied to determine predictors of a rise in serum creatinine of 44.2 mumol/L or more. The baseline serum creatinine level and age were significant predictors of renal injury, but hypertension, diabetes mellitus, congestive heart failure, vascular disease, the volume of contrast agent injected or baseline values of urinary variables did not predict nephrotoxicity. In an independent validation sample, only the baseline serum creatinine level was confirmed as a predictor of nephrotoxicity, whereas age was not. A model that predicted contrast-induced nephropathy by the serum creatinine level showed an exponential increase in the risk for nephrotoxicity if the baseline level was 106.1 mumol/L or higher. Conclusions Patients have a small but significant rise in serum creatinine after cardiac catheterization with a nonionic contrast agent. Baseline renal insufficiency is the only confirmed predictor of nonionic contrast-induced nephrotoxicity.