Contribution of the left atrial remodeling to the elevated pulmonary capillary wedge pressure in patients with WHO Group II pulmonary hypertension.

BACKGROUND: The contribution of progressive left atrial (LA) enlargement to elevated pulmonary capillary wedge pressure (PCWP) in patients with WHO Group II pulmonary hypertension (PH) has not been well studied. We hypothesized that progressive LA enlargement is associated with increased PCWP. METHODS: A cross-sectional retrospective cohort consisted of 166 patients with HF and WHO Group II PH, confirmed by right heart catheterization (RHC). LA anteroposterior dimension and volume were measured on TTE. PCWP and other hemodynamic parameters were measured by RHC. Univariate and multivariate logistic regression models were used for analysis. RESULTS: LA enlargement was associated with advanced age, increased BMI, and LV ejection fraction < 40%. PCWP was progressively increased in patients with dilated LA: 16.9 ± 7.4 mmHg in normal LA, 17.6 ± 7.2 mmHg in mildly dilated LA, 22.6 ± 6.3 mmHg in moderately and 22 ± 7.6 in severely dilated LA (p < 0.001). In multiple logistic regression, after adjustment for echocardiographic and clinical variables, severe LA enlargement was independently predictive of elevated PCWP (OR 3.468; 95% CI 1.046-11.504; p = 0.042). After excluding significant mitral regurgitation, progressive LA dilatation was associated with higher PCWP V-wave amplitude: from 21.3 ± 10.4 mmHg in patients with normal LA size, to 30.9 ± 11.7 mmHg in moderately dilated and 31.0 ± 11.6 mmHg in severely dilated LA (p < 0.001). CONCLUSIONS: In patients with HF and WHO Group II PH, progressive LA enlargement was independently associated with elevated PCWP. After excluding significant mitral regurgitation, LA enlargement was also associated with increased V-wave amplitude, indicative of decreased atrial compliance.

Streptococcus pyogenes meningitis and endocarditis in a patient with prosthetic mitral valve.

Streptococcus pyogenes is commonly found in cutaneous and pharyngeal infections, but rarely causes meningitis and endocarditis. We report a 77-year-old male with history of prosthetic mitral valve, presenting with meningitis and endocarditis secondary to S. pyogenes. We aim to raise awareness among clinicians of rare infectious etiology as the cause of endocarditis and meningitis, and importance of prompt diagnosis in ensuring success of medical treatment and long-term survival. .

Acute Coronary Syndrome: An Unusual Consequence of GERD.

We report a case of an 83-year-old man with history of coronary artery disease and gastroesophageal reflux disease (GERD) who presented with sudden onset nocturnal dyspnea. He was diagnosed with non-ST elevation myocardial infarction based on the electrocardiographic changes and cardiac biomarker elevation. Cardiac catheterization revealed chronic three-vessel coronary artery disease, with 2 patent grafts and 2 chronically occluded grafts. While at the hospital, the patient experienced a similar episode of nocturnal dyspnea, prompting a barium esophagram, which was suggestive of a stricture in the distal esophagus from long-standing GERD. We hypothesized that he had myocardial ischemia due to increased oxygen demand from uncontrolled GERD symptoms. He had no further ischemic episodes after increasing the dose of antireflux medication over a 6-month follow-up. After presenting our case, we review the literature on this atypical presentation of GERD causing acute coronary syndrome and discuss potential mechanisms.

Lyme Carditis in the Fast Lane: From Alternating Bundle Branch Block to Asystole in 12 Hours.

Lyme borreliosis is a multisystem infectious disease with well-known cardiac involvement, including potential carditis as well as conduction abnormalities. We report a case of Lyme disease in a previously healthy 24-year-old male presenting with alternating right- and left-bundle branch block, indicating infra-Hisian atrioventricular (infra-His) block with an accelerated fascicular escape rhythm. Inless than 12 hours, the conduction abnormalities progressed to asystole requiring the urgent placement of a temporary transvenous pacemaker. Subsequently, with appropriate antibiotic treatment, the patient's conduction abnormalities resolved in a week without the need for a permanent pacemaker.

Revascularization options in stable coronary artery disease: it is not how to revascularize, it is whether and when to revascularize.

Patients with acute coronary syndromes and severe multivessel or left main coronary artery disease have better outcomes when prompt revascularization is performed in addition to optimal medical therapy (OMT). However, in patients with stable ischemic heart disease, randomized strategy trials have revealed equipoise between initial strategies of OMT alone and OMT plus revascularization. Conducted in diverse stable ischemic heart disease patient populations and throughout the spectrum of atherosclerotic and ischemic burden, the RITA-2, MASS II, COURAGE, BARI 2D and FAME 2 trials demonstrate that OMT alone and OMT plus revascularization yield similar outcomes with respect to mortality and myocardial infarction. What remains unclear is whether there may be one or more subsets of patients with stable ischemic heart disease in whom revascularization may be associated with a reduction in mortality or myocardial infarction, which is to be addressed in the ongoing ISCHEMIA trial.

The impact of weight loss on cardiac structure and function in obese patients.

BACKGROUND: Obesity frequently results in structural and physiologic changes in the cardiovascular system. Whether weight reduction leads to reversal of these changes is not well-established. This investigation sought to identify the effect of a weight reduction program on right and left ventricular structure and function. METHODS: Sixty-two patients presenting to the eating disorders clinic at a single academic institution for weight loss programs were prospectively enrolled. Baseline and follow-up transthoracic echocardiograms were obtained after at least 10% weight reduction or 6 months after baseline echocardiogram. Complete 2-dimensional echocardiograms were performed with M-mode, flow Doppler, and tissue Doppler evaluation. RESULTS: Patients lost an average of 28.2 +/- 3 kg over a period of 266 +/- 36 days. Left ventricular mass decreased significantly from 255.87 +/- 12 to 228 +/- 11 gm. There were no statistically significant changes in contractility or diastolic indices. The ratios of early-to-late diastolic mitral inflow velocities (E/A) increased from 1.30 +/- 0.05 to 1.32 +/- 0.06. The ratio of early mitral flow to early annular velocity (E/Em) also increased from 5.57 +/- 0.22 cm to 5.82 +/- 0.23 cm. Deceleration time increased from 213.26 +/- 5.3 s to 228.47 +/- 5.7 s. CONCLUSIONS: Weight reduction is associated with decrease in left ventricular diastolic size and left ventricular mass. This weight reduction is not associated with statistically significant improvement in systolic or diastolic function.

Postoperative hyperbilirubinemia is an independent predictor of longterm outcomes after cardiopulmonary bypass.

BACKGROUND: Two decade-old studies of cardiopulmonary bypass (CPB) patients documented a 25% to 35% incidence of postoperative hyperbilirubinemia, associated with increased in-hospital morbidity and mortality. Longterm consequences of this complication are unknown. STUDY DESIGN: Medical records of CPB patients were reviewed. Mortality was ascertained through the National Death Index. Proportional hazards determined important factors in post-CPB survival. Logistic regression delineated predictors of hyperbilirubinemia. Kaplan-Meier and Mantel-Cox log-rank survival analyses compared hyperbilirubinemia groups. RESULTS: Bilirubin levels were followed in 826 (59.7%) patients. Bilirubin was normal in 570 (69.0%) patients (group 1), it was 1.4 to 2.8 mg/dL in 184 (22.3%) patients (group 2), and it exceeded 2.8 mg/dL in 72 (8.7%) patients (group 3). Elevated bilirubin was associated with decreased body mass index, congestive heart failure, heparin before operation, postoperative transfusion requirement, bleeding, and renal failure. In-hospital mortality was 4.3% in group 2 and 25.0% in group 3, compared with 0.9% in group 1 (p<0.001). Two-year crude survival was 95.8% in group 1, 84.8% in group 2, and 62.5% in group 3 (p<0.001). Multivariable predictors of longterm mortality were older age, history of stroke, emergency operation, increased duration of cardiopulmonary bypass, respiratory failure, and elevated bilirubin. Compared with survival in group 1, there was a 1.7-fold decrease in group 2 2-year survival (95% CI 0.9 to 3.0; p=0.09) and a 3.8-fold decrease in group 3 survival (95% CI 2.0 to 7.2; p<0.001). CONCLUSIONS: Postoperative bilirubin elevation in CPB patients is common and deadly. The predictive power of hyperbilirubinemia is similar to that of respiratory failure. The cause of postbypass hyperbilirubinemia is unknown and is probably multifactorial. Additional prospective studies are warranted.

African Americans with LVH demonstrate depressed sensitivity of the coronary microcirculation to stimulated relaxation.

Excess coronary heart disease morbidity and mortality among African Americans remains an important yet unexplained public health problem. We hypothesized that adverse outcome is in part due to intrinsic or acquired abnormalities in coronary endothelial function and vasoreactivity. We compared dose-response curves relating changes in coronary blood flow and epicardial diameter to graded infusions of acetylcholine in 50 African American and 65 white subjects with hypertensive left ventricular hypertrophy (LVH) and normal coronary arteries. These groups were similar for age, body mass index, mean arterial pressure, and indexed left ventricular mass. The same protocol was conducted in 24 normotensive African American and 56 similar white subjects. We found significant depression in the coronary blood flow dose-response curve relation among African Americans when compared with white subjects with similar LVH (P<0.03). Racial differences were observed at all doses of acetylcholine but were less precisely estimated at the highest dose. The same testing among normotensive subjects revealed similar dose-response curves with no significant effect of race. Qualitatively similar results were found with respect to coronary diameter. Adenosine responses, a measure of endothelium-independent function, were similar after partitioning by LVH. Our study demonstrates that there are racial differences in sensitivity of coronary arteries to acetylcholine-stimulated relaxation among those with LVH. These results provide a mechanism whereby racial differences in coronary vasoreactivity might contribute to adverse coronary heart disease outcome among African Americans, a group in whom LVH is prevalent.

The presence of African American race predicts improvement in coronary endothelial function after supplementary L-arginine.

OBJECTIVES: The purpose of our study was to determine if the presence of African American ethnicity modulates improvement in coronary vascular endothelial function after supplementary L-arginine. BACKGROUND: Endothelial dysfunction is an early stage in the development of coronary atherosclerosis and has been implicated in the pathogenesis of hypertension and cardiomyopathy. Amelioration of endothelial dysfunction has been demonstrated in patients with established coronary atherosclerosis or with risk factors in response to infusion of L-arginine, the precursor of nitric oxide. Racial and gender patterns in L-arginine responsiveness have not, heretofore, been studied. METHODS: Invasive testing of coronary artery and microvascular reactivity in response to graded intracoronary infusions of acetylcholine (ACh) +/- L-arginine was carried out in 33 matched pairs of African American and white subjects with no angiographic coronary artery disease. Pairs were matched for age, gender, indexed left ventricular mass, body mass index and low-density lipoprotein cholesterol. RESULTS: In addition to the matching parameters, there were no significant differences in peak coronary blood flow (CBF) response to intracoronary adenosine or in the peak CBF response to ACh before L-arginine infusion. However, absolute percentile improvement in CBF response to ACh infusion after L-arginine, as compared with before, was significantly greater among African Americans as a group (45 +/- 10% vs. 4 +/- 6%, p = 0.0016) and after partitioning by gender. The mechanism of this increase was mediated through further reduction in coronary microvascular resistance. L-arginine infusion also resulted in greater epicardial dilator response after ACh among African Americans. CONCLUSIONS: We conclude that intracoronary infusion of L-arginine provides significantly greater augmentation of endothelium-dependent vascular relaxation in those of African American ethnicity when compared with matched white subjects drawn from a cohort electively referred for coronary angiography. Our findings suggest that there are target populations in which supplementary L-arginine may be of therapeutic benefit in the amelioration of microvascular endothelial dysfunction. In view of the excess prevalence of cardiomyopathy among African Americans, pharmacologic correction of microcirculatory endothelial dysfunction in this group is an important area of further investigation and may ultimately prove to be clinically indicated.