Background: Systolic time intervals measured by echocardiography and carotid artery tracings are validated methods of assessing left ventricular function. However, the clinical utility of ...phonoelectrocardiographic systolic time intervals for predicting heart failure using newer technology has not been evaluated.
Methods: We enrolled 100 adult patients undergoing left heart catheterization. Participants underwent computerized phonoelectrocardiographic analysis, left ventricular end‐diastolic pressure (LVEDP) measurement, transthoracic echocardiographic measurement of left ventricular ejection fraction (LVEF), and B‐type natriuretic peptide (BNP) testing. The heart rate‐adjusted systolic time intervals included the time from the Q wave onset to peak S1 (electromechanical activation time, EMAT), Q wave onset to peak S2 (electromechanical systole, Q‐S2), and peak S1 to peak S2 (left ventricular systolic time, LVST). Left ventricular dysfunction was defined as the presence of both LVEDP >15 mmHg and LVEF <50%.
Results: EMAT (r =−0.51; P < 0.0001), EMAT/LVST (r =−0.41; P = 0.0001), and Q‐S2 (r =−0.39; P = 0.0003) correlated with LVEF, but not with LVEDP. An abnormal EMAT ≥15 (odds ratio 1.38, P < 0.0001) and EMAT/LVST ≥0.40 (OR 1.13, P = 0.002) were associated with left ventricular dysfunction. EMAT ≥15 had 44% sensitivity, 94% specificity, and a 7.0 likelihood ratio for left ventricular dysfunction, while EMAT/LVST ≥0.40 had 55% sensitivity, 95% specificity, and a 11.7 likelihood ratio. In patients with an intermediate BNP (100–500 pg/mL), the likelihood ratio increased from 1.1 using the BNP result alone to 11.0 when adding a positive EMAT test for predicting left ventricular dysfunction.
Conclusions: Phonoelectrocardiographic measures of systolic time intervals are insensitive but highly specific tests for detecting abnormalities in objective markers of left ventricular function. EMAT and EMAT/LVST provide diagnostic information independent of BNP for detecting patients with left ventricular dysfunction.
Although an inverse relationship between dehydroepiandrosterone sulfate (DHEAS) and coronary artery disease has been demonstrated in men, the vascular effects of DHEAS are not well defined. The ...vasoactive effects of intracoronary DHEAS and testosterone (0.1 nM to 1 microM) were examined in vivo in 24 pigs. Epicardial cross-sectional area was measured by intravascular ultrasound, and coronary flow velocity by intravascular Doppler velocimetry. We also examined the effects of antagonism of the androgen receptor, nitric oxide synthase, and potassium channels on DHEAS-induced vasodilation in vitro in coronary rings from male and female pig hearts. DHEAS and testosterone induced increases in cross-sectional area, average peak velocity, and coronary blood flow. The maximal increase in coronary blood flow in response to testosterone was 1.26-fold (P=0.02), and in average peak velocity 1.43-fold (P=0.05), greater than that to DHEAS, whereas increases in cross-sectional area were similar. Vasodilation to both hormones was rapid, with maximal responses occurring <10 minutes after administration. In vitro, DHEAS and testosterone induced vasodilation in coronary rings, greater with testosterone. At doses of 0.1 and 1 microM, the vasodilator effects of DHEAS and testosterone were inhibited by the androgen receptor antagonist flutamide but not the estrogen receptor antagonist ICI 182,780. At 10 microM, neither DHEAS- nor testosterone-induced vasorelaxation was inhibited by flutamide, ICI 182,780, L-NAME, or deendothelialization, but both were attenuated by pretreatment with glibenclamide. No gender differences were observed in any of the responses examined. In conclusion, DHEAS is an acute coronary artery vasodilator, but less potent than testosterone. Its effect might be mediated via androgen receptors and may involve ATP-sensitive potassium channels.
To determine whether secondhand smoke (SHS) induces pulmonary artery endothelial dysfunction, and whether dietary l-arginine supplementation is preventive.
SHS causes coronary and peripheral arterial ...endothelial dysfunction.
The effects of l-arginine supplementation (2.25% solution) and SHS (10 weeks) on pulmonary vascular reactivity were examined in 32 rabbits fed a normal diet. Endothelium-dependent relaxation of precontracted pulmonary artery segments was studied using acetylcholine and calcium ionophore. Endothelium-independent relaxation was studied using nitroglycerin. Endothelial and serum l-arginine levels were measured by chromatography. In eight SHS-exposed and in eight control rats, pulmonary artery nitric oxide synthase (NOS) activity and arginase activity were studied using the titrated arginine to citrulline conversion assay.
SHS reduced maximal acetylcholine-induced (p = 0.04) and calcium ionophore-induced (p = 0.02) relaxation. l-Arginine increased maximal acetylcholine-induced (p = 0.047) vasodilation. SHS and l-arginine did not influence nitroglycerin-induced relaxation. SHS reduced endothelial l-arginine (p = 0.04) but not serum l-arginine. l-Arginine supplementation increased endothelial (p = 0.007) and serum l-arginine (p < 0.0005). Endothelium-dependent relaxation induced by acetylcholine and calcium ionophore varied directly with endothelial (r = 0.67, r = 0.67) and serum l-arginine (r = 0.43, r = 0.45), respectively. SHS reduced constitutive NOS activity (p = 0.03).
SHS reduces pulmonary artery endothelium-dependent relaxation by decreasing NOS activity and possibly by decreasing endothelial arginine content. l-Arginine supplementation increases serum and endothelial l-arginine stores and prevents SHS-induced endothelial dysfunction. l-Arginine may offset the deleterious effect of SHS on pulmonary arteries by substrate loading of the nitric oxide pathway.
Hyponatremia
has been identified as a risk factor for increased morbidity and
mortality in patients with congestive heart failure (CHF) and other
edematous disorders and can lead to severe neurologic ...derangements. Low
cardiac output and blood pressure associated with CHF triggers a
compensatory response by the body that activates several neurohormonal
systems designed to preserve arterial blood volume and pressure.
Hyponatremia in patients with CHF is primarily caused by increased
activity of arginine vasopressin (AVP). AVP increases free-water
reabsorption in the renal collecting ducts, increasing blood volume and
diluting plasma sodium concentrations. Hyponatremia may also be
triggered by diuretic therapy used in the management of symptoms of
CHF. Hyponatremic disorders occur when the normal ratio of solutes to
body water content is altered by parallel changes in serum sodium and
osmolality. Hyponatremia is generally defined as a serum sodium ion
concentration <135 to 136 mmol/L and can be broadly categorized into
2 types, dilutional or depletional. Dilutional hyponatremia is the most
common form of hyponatremia and is caused by excess water retention.
Depletional hyponatremia is usually hypovolemic, with an absolute
deficiency of water but a relative excess of body water compared with
sodium
concentration.
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