Unusual Delayed Manifestation of a Penetrating Chest Trauma

Abstract Pericardial tamponade remains a diagnostic challenge to the clinician especially when the patient is well compensated hemodynamically. We report an unusual case who sought medical help 1 month after having been stabbed in his chest. An investigation revealed a perforation of the myocardium and a pericardial tamponade. The patient survived thanks to a large organized clot that plugged the perforation. The patient was exposed to increased risk due to delayed onset, recognition, and therapy of the tamponade. Most reports on this subject deal with acute pericardial tamponade. Only few cases of delayed pericardial tamponade have been reported. A review of the relevant literature and the therapeutic approaches are discussed.     

The J-curve relationship of treated diastolic blood pressure to mortality risk: Is it real? Is it clinically meaningful?

Low diastolic blood pressure is alleged to impose excess cardiovascular disease (CVD) risk in patients with treated hypertension, impeding aggressive reduction of blood pressure. Most investigations that assessed the potential J-shaped relations of diastolic blood pressure and adverse outcomes have not adequately considered systolic or pulse pressure in statistical analyses. An overview of hypertension trials indicates that lowering elevated blood pressure reduces the risk of CVD outcomes irrespective of the associated decrease in diastolic pressure, even if the achieved diastolic pressure averages less than 70 mm Hg. The Framingham study investigations have determined that the increased CVD incidence observed at low diastolic blood pressure levels is confined largely to persons with concomitantly increased systolic pressure. This finding of no true excess risk at low diastolic blood pressure agrees with the results of trials that have evaluated the J-curve phenomenon adjusting for systolic pressure. Aggressively treating systolic hypertension appears to produce no cause for alarm.     

Guanylnucleotide specificity for muscarinic receptor inhibitory coupling to cardiac adenylate cyclase.

The guanylnucleotide specificity of muscarinic acetylcholine receptor (MR) inhibitory coupling to cardiac adenylate cyclase (AC) was investigated under low MgCl2 (i.e., 0.5 mM) conditions. In purified cardiac sarcolemma, carbachol maximally inhibited AC activity 60% in the presence of GTP. Carbachol-dependent inhibition in the presence of guanosine 5'-O-(3-thiotriphosphate (GTP gamma S) or guanylylimidodiphosphate [Gpp(NH)p] was of lesser magnitude (i.e., 30%) and was evident only during short incubation periods. Of greater interest, carbachol maximally inhibited AC activity in the presence of GDP and guanosine 5'-O-(2-thiodiphosphate (GDP beta S) by 35 and 60%, respectively. Control studies ruled out transphosphorylation of GDP and GDP beta S by nucleoside diphosphate kinase or guanylnucleoside triphosphate contamination as reasons for the inhibitory effects of GDP and GDP beta S. Furthermore, isoproterenol stimulated AC in the presence of GTP, GTP gamma S, and Gpp(NH)p but not in the presence of GDP or GDP beta S. Therefore, GDP and GDP beta S may serve as agonists on MR-activated Gi but not on beta-adrenergic receptor-activated Gs in these membranes. Time course studies revealed that carbachol-dependent inhibition of AC in the presence of either GTP or GDP occurred without a detectable lag period, and this inhibition was rapidly reversed by atropine. In contrast, a 1-2-min lag time was required for carbachol- and GDP beta S-dependent inhibition of AC to occur, and inhibition, once developed, was only partially and slowly reversed by atropine. Preincubation of sarcolemma with carbachol and GDP beta S, in the absence of ATP or under nonphosphorylating conditions, eliminated the lag time for inhibition of AC activity. Although it is unlikely that GDP and GDP beta S have physiological relevance of MR-Gi-AC coupling, these studies provide unique insights into this coupling mechanism in cardiac membranes.     

Metabolic Syndrome and Inflammatory Biomarkers: a community-based cross-sectional Study at the Framingham Heart Study

ABSTRACT: BACKGROUND: Prior studies reported conflicting findings on the association between metabolic syndrome and inflammatory biomarkers. We tested the cross-sectional association between metabolic syndrome, its components, and 9 inflammatory markers. METHODS: We measured C-reactive protein, CD40 ligand, interleukin-6, intercellular adhesion molecule-1, monocyte chemoattractant protein-1, osteoprotegerin, P-selectin, tumor necrosis factor-alpha, and tumor necrosis factor receptor-2 in 2570 Framingham Offspring Study participants free of diabetes and cardiovascular disease at exam 7. Metabolic syndrome was defined by criteria of the National Cholesterol Education Program. We performed multivariable linear regressions for each biomarker with metabolic syndrome as the exposure adjusting for age, sex, smoking, aspirin use, and hormone replacement. We subsequently added each component of the metabolic syndrome as a continuous trait to the models, adjusting for age, sex, smoking, aspirin use, hormone replacement, lipid lowering treatment and hypertension therapy. We considered P < 0.05 as statistically significant. RESULTS: Metabolic syndrome was present in 984 participants, and statistically significantly associated with each biomarker (all P<0.0001) except osteoprotegerin. After adjusting for its components, the metabolic syndrome was only associated with P-selectin (beta=0.16, 95% CI (0.05, 0.27)). CONCLUSIONS: Metabolic syndrome was associated with multiple inflammatory biomarkers. However, adjusting for each of its components eliminated the association with most inflammatory markers, except P-selectin. Our results support the hypothesis that the relation between metabolic syndrome and inflammation is largely accounted for by its components.     

Cross-sectional relations of urinary sodium excretion to cardiac structure and hypertrophy. The Framingham Heart Study

BACKGROUND: Increased sodium intake has been positively associated with high blood pressure (BP) and hypertensive target organ damage, but associations with cardiac structure in nonhypertensive individuals have yielded inconsistent results. We tested the hypothesis that sodium intake is associated with left ventricular (LV) mass and left ventricular hypertrophy (LVH), independent of BP, in the community. METHODS: We analyzed the cross-sectional relationships between urinary sodium excretion and LV measurements in a community-based sample of 2660 Framingham Offspring Study participants (mean age 58 years, 56% women and 44% men). Participants with known coronary artery disease, congestive heart failure, or renal failure as well as those using diuretics were excluded. Urinary sodium excretion was measured on a spot urine sample and was indexed to urinary creatinine. RESULTS: In sex-specific, multivariable linear regression models adjusting for covariates known to influence LV measurements, log urinary sodium was not associated with LV mass, wall thickness, end-diastolic dimensions, or left atrial size in either sex. Urinary sodium was not related to LVH defined as LV mass >/= sex-specific 80th percentile value. In analyses restricted to hypertensive individuals (n = 983, 470 women), urinary sodium was not associated with LV mass or LVH. CONCLUSIONS: In our large community-based sample, urinary sodium excretion was not related to LV mass, function, or hypertrophy.