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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.

Acute stress cardiomyopathy (ASC), also known as broken heart syndrome, has become increasingly recognized among patients presenting with suspected acute coronary syndrome since it was first described in Japan in 1990. The classic presentation is most common in older females following emotional or

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.

Recent reports suggest aortoembolism is an important cause of stroke. Although transesophageal echocardiography visualizes the aortic arch, diagnosis of aortoembolism stroke is not common. We investigated reasons for this discrepancy at our institution. We reviewed charts and transesophageal echocardiography videotapes of 16 patients with recent ischemic stroke or transient ischemic attack who had undergone transesophageal echocardiography. For each patient, we determined the most likely cause of cerebral ischemia, and we compared the official transesophageal echocardiography report to our interpretation of the videotape. In our videotape review, 13 patients had good visualization of the aortic arch. Of 6 patients with atherosclerosis in the arch, 1 had high-grade carotid stenosis, 1 had atrial fibrillation, 1 had "small-vessel disease," and 3 had cerebral ischemia of unknown cause. The official reports did not mention aortic arch disease in 4 of 6 patients. A possible cause of cerebral ischemia was identified in 6 of 7 patients with normal aortic arches. Of 3 patients who had poor visualization of the aortic arch, one had "small-vessel disease," and 2 had ischemic stroke of unknown cause despite extensive workups. We conclude that aortic arch disease is common in patients with ischemic stroke and transient ischemic attack and may be a cause of cerebral ischemia, especially in patients with stroke or transient ischemic attack due to small-vessel occlusion or of unknown cause. Aortic arch disease may not be identified as the cause of stroke or transient ischemic attack because (a) transesophageal echocardiography is not done, (b) transesophageal echocardiography is done but the aortic arch is not visualized, (c) transesophageal echocardiography is done, the aortic arch is visualized, but the examiner does not comment on aortic arch disease, or (d) despite transesophageal echocardiography identification of arotic arch disease, the treating physician does not consider the aorta to be a potential source of embolization.

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.

The overall objective of this study was to determine the role fructose 1,6-diphosphate (FDP), a naturally occurring glycolytic intermediate, plays in activated T-lymphocytes. The hypothesis is twofold. First, we propose that FDP inhibits T cell proliferation to a greater extent than fructose-1-phosphate (F1P), fructose-6-phosphate (F6P) and mannose-6-phosphate (M6P); second, we argue that FDP suppresses immune activation by inhibiting inflammatory cytokine expression, inhibiting expression of key transcription factors, and by inducing apoptosis in immune cells. Rat spleen cells were incubated with concanavalin A (ConA) and increasing concentrations of FDP. Proliferation was determined by tritiated thymidine uptake. FDP inhibited splenocyte proliferation in a dose-related manner while F1P, F6P, M6P demonstrated inhibition only at high concentrations (5000 microg/ml). RNA was harvested from FDP and ConA-treated cells and IL-1 and IL-6 gene expression was analyzed by RT-PCR. IL-1 and IL-6 mRNA expression was completely inhibited at 500-5000 microg/ml FDP. Apoptosis in FDP-treated lymphocytes was determined by DNA fragmentation and flow cytometry. Propidium iodide (PI) staining demonstrated a 39% rate of apoptosis in splenocytes treated with ConA and 5000 microg/ml FDP. Extensive DNA fragmentation was present at 250-5000 microg/ml FDP, and maximal inhibition occurred at 5 microg/ml. F1P, F6P and M6P showed maximal inhibition only at 5000 microg/ml. Nuclear extracts from FDP-treated splenocytes were analyzed by electrophoretic mobility shift assay. ConA activation of NF-kappaB and AP-1 was dramatically inhibited by FDP. Interestingly, beta-actin showed extensive inhibition with FDP and ConA, thus suggesting new possibilities of its being used as a therapeutic modality in arterial injury where the beta-actin, an important cytoskeleton element, plays a very important role. These data indicate that FDP may be a useful immunosuppressive agent. In conclusion, FDP is not only an immunosuppressant but also an anti-inflammatory agent.

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.

Previously, we reported that elevated extracellular potassium concentration in vitro inhibited proliferation and migration of vascular smooth muscle cells, formation of free radical compounds by macrophages, and reduced platelet sensitivity to agonists. More recently, we described a reduction in neointimal proliferation after balloon angioplasty injury in the carotid arteries of rats associated with an elevation of dietary potassium intake during a 4-week experiment. In the present study we conducted a similar investigation in the swine coronary artery balloon angioplasty model.Two groups of seven castrated male swine were studied; for 28 days the normal potassium group consumed a diet containing 0.25% potassium and the high potassium group ate diet containing 2.0% potassium. After 14 days on the diet, balloon angioplasty was performed. After an additional 14 days on the same diets the hearts were removed, and normal and lesioned sections of the artery were analyzed histologically.The neointimal area was markedly less in the high potassium group than in the normal potassium group, 0.33+/-0.04 mm2 v 0.74+/-0.10 mm2 (P.004). Neointimal area-to-total wall area ratio in the normal potassium group averaged 0.199+/-0.018, significantly greater than the ratio computed for the elevated potassium group, 0.120+/-0.015 (P.006).These results support the hypothesis that a high level of dietary potassium intake inhibits neointimal proliferation after balloon angioplasty in the swine coronary artery.

Left ventricular false tendons (LVFTs) are chord-like structures that traverse the LV cavity and are generally considered to be benign. However, they have been associated with arrhythmias, left ventricular hypertrophy and LV dilation in some small studies. Our objective was to evaluate the

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: The association between left atrial (LA) size, ischemic stroke and mortality has been investigated in non-Hispanic whites but not in African Americans despite their disproportionately higher rates of stroke and cardiovascular mortality. Purpose: We examined the association of LA size assessed by echocardiogram with the incidence of ischemic stroke and all-cause mortality in a large population-based cohort of African Americans. Methods: Participants in the Jackson cohort of the ARIC study have been extensively evaluated including echocardiograms during the third examination (1993–1995) and have been followed for incident cardiovascular events including stroke. Results: The study population consisted of 1,887 participants of which 660 (35%) were men with a mean age of 58.9 ± 5.7 years. LA diameter by tertile was significantly related to hypertension, diabetes and body mass index (BMI) (p Conclusions: In this middle-aged population based cohort of African Americans, LA size was significantly associated with all-cause mortality independent of traditional cardiovascular risk factors.

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.

Patent foramen ovale (PFO) is common occurring in approximately 10-35% of patients. Paradoxical emboli are less so, but we presume that a paradoxical embolism causes cryptogenic stroke in patients with a PFO. It is rare to find a thrombus in transit. Case Description: 62 year old male presented

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.

Background Cardiovascular disease (CVD) is the leading cause of death in the United States. In comparison to whites, African-Americans have a higher risk of dying from CVD and have a worse risk factor profile. The Jackson Heart Study (JHS) is designed to investigate the origin and natural history of CVD in African-Americans. Methods Reading centers for electrocardiograms, echocardiograms, carotid ultrasonograms, pulmonary function tests, and ambulatory blood pressure monitoring provide training for data accrual, quality assurance assessments, and specialized measurements for research objectives. Laboratories adhering to well-established quality assurance programs provide blood and urine analyses, as well as storage of specimens for future assays. A new Coordinating Center was created to perform functions analogous to those of coordinating centers for multisite studies, including protocol development, data management, statistical analyses, and operational support for the study. An established coordinating center serves as a resource to the JHS Coordinating Center, providing assistance in preparing procedure manuals and data collection forms. This group also designed and developed the JHS data management system. Results This network of specialized research organizations is implementing state- of-the-science methodologies to assess prevalence, progression, and incidence of CVD and subclinical atherosclerosis, and to evaluate a myriad of risk factors. From November 2000 through March 2004, JHS collected 4000 data fields on each of more than 5300 African-American participants. Conclusions This article describes the roles of specialized research agencies contributing to JHS, and the methodologies being utilized to accumulate study data. A diverse collection of scientific disciplines is required to collect the information needed to meet the objectives of the JHS.

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

Ubiquitous viruses such as members of the human herpes virus group, particularly cytomegalovirus (CMV), have been proposed to be clinically important agents in the initiation and progression of atherosclerosis. Antibodies to CMV and herpes simplex virus type 1 (HSV1) and type 2 (HSV2) were determined in 340 matched case-control pairs from the Atherosclerosis Risk in Communities (ARIC) Study. Cases were defined by B-mode ultrasonography as persons with thickened carotid artery walls consistent with early atherosclerosis but without a history of cardiovascular disease. Controls were defined as persons without thickened walls or history of cardiovascular disease. The case-control odds ratio for CMV antibodies was 1.55 (P = 0.03), for HSV 1.41 (P = 0.07), and for HSV2 0.91 (P = .63). When adjustment was made for potential con-founders, the odds ratios were 1.36 for CMV (P=.24), 1.21 for HSV1 (P = .45), and 0.61 (P = .05) for HSV2. These results suggest a modest association between CMV and asymptomatic carotid wall thickening consistent with early atherosclerosis. © 1994 Wiiey-Liss, Inc.

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.

Fructose-1,6-diphosphate (FDP) is reported to have a salutary effect in endotoxin shock and sepsis. This investigation describes the effect of FDP on pulmonary and systemic hemodynamics, lung lymph protein clearance, and leukocyte count in sheep infused with Escherichia coli endotoxin.Anesthetized sheep (n = 18), some of which underwent thoracotomy to cannulate lymphatic nodes, were used in this study. After stabilization, all sheep received E. coli endotoxin, 5 microg/kg i.v. infusion over 30 min. Concomitant with the endotoxin infusion, half of the animals were randomly selected to receive an i.v. bolus of FDP (10%), 50 mg/kg, followed by a continuous infusion of 5 mg.kg(-1).min(-1) for 4 h; the rest were treated in the same manner with glucose (10%) in 0.9% NaCl.Pulmonary artery pressure (PAP) and resistance in the glucose group increased from 20.8 +/- 1.6 to 36.7 +/- 3.2 mmHg (P0.007) and from 531 +/- 114 to 1137 +/- 80 dyn.s(-1).cm(-5), respectively (P0.005). Despite an increase during endotoxin infusion, these parameters in the FDP group returned to control values. There were no differences in left ventricular pressures, cardiac output, heart rate, and arterial oxygen tension between the groups. In the glucose group, lymph protein clearance was higher (P0.01) and blood leukocyte count was lower (P0.02). The wet/dry lung weight ratio (g/g) for the glucose group was 5.57 +/- 0.04 and for the FDP-treated group 4.76 +/- 0.06 (P0.0005).FDP treatment attenuated significantly the characteristic pulmonary hypertension, lung lymph protein clearance, and pulmonary vascular leakage seen in sheep infused with endotoxin.

A male 34-year-old hypertensive smoker with hypertension, hepatitis C, and a history of multiple drug abuse presented to the emergency department with malaise, fever, and chills for approximately 1 week. Physical examination revealed a systolic ejection murmur heard throughout the precordium. Labwork showed leukocytosis, mild normocytic anemia, and thrombocytosis. Radiography revealed mild cardiomegaly and a left pleural effusion as well as a 2 cm nodule in the right midlung and a 2 × 5 cm mass in the left lower lobe. He was admitted and started on empiric antibiotic therapy. Initial blood cultures returned Staphylococcus epidermidis and Acinetobacter baumannii. Computed tomography of the chest was performed to evaluate the pulmonary masses and showed multiple peripheral masses in both lungs; also noted was a right atrial mass. Echocardiography was performed to better characterize the atrial mass and demonstrated a mass in the right atrium measuring 2.6 × 3.9 cm as well as a mass along the posterior wall of the right ventricle measuring 1.3 × 1.4 cm with severe left ventricular systolic dysfunction. Echocardiography-guided biopsy of the right atrial mass was consistent with thrombus. Anticoagulation was initiated with enoxaparin and warfarin. He was discharged home after 3 weeks of antibiotic therapy on warfarin, carvedilol, lisinopril, and intravenous vancomycin and levofloxacin with plans to continue intravenous antibiotics for a total of 6 weeks. Two weeks following discharge, he was seen in follow-up and had repeat blood cultures, which were sterile. Six weeks following discharge, a repeat echocardiogram showed mild left ventricular systolic dysfunction with an ejection fraction of 45%; there was no indication of a mass or thrombus in either the right atrium or right ventricle. Intracardiac masses are uncommon, occurring in less than 0.1% of autopsies. The differential diagnosis of these masses is broad and includes myxomas, papillary fibroelastomas, lipomatous hypertrophy of the atrial septum, thrombi, and malignancies (either primary or metastatic). Although left ventricular thrombi are commonly noted, particularly with severe left ventricular systolic dysfunction and following myocardial infarction, and right atrial thrombi are often noted (particularly in the presence of pulmonary embolism), right ventricular thrombi are exceedingly rare. To our knowledge, this is the first case report of what we assume to be right ventricular thrombus in situ related to sepsis.

A 52-year-old female with hypertension and type 2 diabetes mellitus presented to the hospital with severe abdominal pain, nausea, and vomiting for 24 hours. On physical examination she had fever and tenderness to palpation in her epigastrium and left upper quadrant. Imaging of her abdomen revealed an ileus. Lab work revealed anemia, severe thrombocytopenia, and acute renal failure; further evaluation showed hypoalbuminemia, hematuria, hyperbilirubinemia, elevated lactate dehydrogenase, and evidence of acute pancreatitis. She was admitted to the hospital for treatment of acute pancreatitis and was given intravenous fluids, antiemetics, and analgesics. Over the next 48 hours she had little improvement in her symptoms; the diagnosis of thrombotic thrombocytopenic purpura (TTP) was made in consultation with a hematologist, and the patient was transferred to a tertiary care hospital for plasmapheresis. Prior to initiation of therapy, however, the patient abruptly developed bradycardia with hypotension and expired. Autopsy findings included nonocclusive coronary artery disease, subepicardial petechiae, endocardial hemorrhage, and vascular microthrombi with associated myocardial necrosis. Sections of lung tissue revealed pulmonary congestion and edema. The characteristic pathological finding in patients with TTP is platelet-rich thrombus formation in the microvasculature of multiple organ systems. Commonly affected tissues include the adrenal glands, pancreas, kidneys, the central nervous system, and the heart. Cardiac involvement is common and was included in the original description of the disorder in 1924 by Moschcowitz. Clinical findings typical of myocardial ischemia are often absent, with a minority of patients reporting chest pain. Cardiac involvement as evidenced by serological myocardial injury biomarkers appears to be more common. Modern therapy with plasmapheresis, with or without the addition of glucocorticoids, has led to a significant reduction in mortality. Despite this improvement in clinical outcomes, histological examination of autopsy specimens shows that myocardial thrombotic involvement likely continues to occur in all patients, and in some cases myocardial infarction is a contributing factor to death. Although it is currently unclear how cardiac injury relates to prognosis in TTP, cardiac monitoring is reasonable given the occasional severity of its effects when myocardium is involved.

Purpose The purpose of this study is to investigate the predictive value of the mitral E/A ratio for morbidity and mortality in a large population-based cohort of middle-aged African Americans. Methods This is a prospective population-based cohort study design. Between 1993 and 1996, participants enrolled in the Jackson (all African American) cohort of the Atherosclerotic Risk in Communities Study received transthoracic echocardiograms, underwent interview and had blood pressure (BP), body mass index (BMI), heart rate (HR), serum lipids and glucose measured. For this study, three subgroups of E/A ratio were defined: E/A ratio 1.5. Study end points included all-cause mortality and CVD events (coronary events and strokes). Cox proportional hazard models were used to assess prognosis of participants with E/A ratio 1.5 compared to those with E/A ratio 0.7-1.5, adjusting for age and gender alone and with BP, HR, BMI, diabetes, lipid status, tobacco use, left ventricular mass and ejection fraction Results The 2,211 participants (65.2% women, mean age = 62 years) had a high prevalence of hypertension, obesity, diabetes and echocardiographic left ventricular hypertrophy (LVH). Adjusting for age and gender, an E/A ratio > 1.5 was predictive of both all-cause mortality (HR 1.74, CI 1.05-2.90; p = .03) and incident CVD (HR 1.75, CI 1.08-2.83; p = .02). An E/A ratio > 1.5 was also independently predictive of all-cause mortality (HR 2.19, CI 1.20-4.02; p = .01) in the multivariable model. An E/A ratio Conclusion In a population-based cohort of middle-aged African Americans where hypertension, obesity and diabetes are epidemic, an E/A ratio > 1.5 independently predicts all-cause mortality. The E/A ratio > 1.5 and an E/A ratio

Cardiac rupture is a rare but devastating complication of myocardial infarction. Free wall rupture, papillary muscle rupture and ventricular septal defect have been described extensively in the literature. Rupture most often occurs in patients with occlusion of a single vessel or severe multivessel coronary artery disease. We describe an unusual case of a 66 year old man who presented to our institution with chest pain of 12 hours duration and ST-segment elevation in leads V4-V6 and II, III and AVF. Echocardiogram revealed an apical ventricular septal defect by Doppler and normal systolic function with apical akinesis. A small pericardial effusion was found as well. Coronary angiography revealed minor luminal irregularities and TIMI 3 flow in all vessels. The right ventricle filled extensively with contrast during left ventriculography. During surgery, the entire free wall of the left ventricle was found to be infarcted. A 2 × 2 mm rupture existed between two large marginal branches. Ventricular septal defects measuring 3 × 3 mm at the apex and mid ventricle were found. The areas of rupture could not be closed due to the extent of surrounding hemorrhage and necrosis. Rupture of the ventricular septum or free wall usually occurs 2 to 4 days after a large infarction and is more common in patients without prior infarction or hypertrophy. Rupture of the anteroapical ventricular septum usually occurs after left anterior descending (LAD) occlusion while rupture of the lateral free wall between obtuse marginal branches occurs after occlusion of the left circumflex or large, dominant right coronary artery. The most remarkable features of this case are (1) near simultaneous rupture in two different vascular territories, (2) absence of angiographically significant coronary disease, (3) early appearance of rupture, within 12 hours of symptom onset, and (4) absence of extensive wall motion abnormality by echocardiography or angiography in the areas of rupture. Possible etiologies of this unusual event include (a) transient occlusion of left main or both the LAD and circumflex arteries due to thrombosis or spasm with reperfusion causing hemorrhage or (b) severe diffuse microvascular obstruction due to thromboemboli or vasospasm.

P70 The insulin resistance syndrome (IRS) has been associated with cardiovascular disease (CVD), 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 African-Americans where both IRS and elevated LV mass are common. Complete information was available for 1633 African-American women and men aged 49-73 who were enrolled in the Atherosclerosis Risk in Communities (ARIC) Study when M-mode echocardiography was performed at one of the four ARIC sites in Jackson, Mississippi (1993-1996). LV mass was calculated according to American Society of Echocardiography methods using the cube formula and was indexed by height. Participants were categorized by the number (0, 1, 2, or 3) of IRS characteristics (hypertension, dyslipidemia (low HDL cholesterol or high triglyceride), and glucose intolerance (diabetes or fasting glucose values ≥110 mg/dl)). Age-adjusted mean LV mass/height (g/m) increased progressively with increasing number of IRS disorders in both women and men (128.9, 148.6, 161.0, 171.6 and 135.9, 157.4, 170.6, 171.6 respectively, p