SummaryBackgroundSome patients with right heart failure develop cardiac hepatopathy (CH). The pathophysiology of CH is thought to be secondary to hepatic venous congestion and arterial ischemia. We sought to define the clinical and hemodynamic characteristics associated with CH.Material/MethodsA retrospective cross sectional analysis was performed in which subjects were identified from our institutional cardiology database if echocardiography showed either right ventricular (RV) hypokinesis or dilatation, and was performed within 30 days of right heart catheterization. A chart review was then performed to identify patient clinical characteristics and to determine if the patients had underlying liver disease. Subjects with non-cardiac causes for hepatopathy were excluded.ResultsIn 188 included subjects, etiology for right heart dysfunction included left heart failure (LHF), shunt, pulmonary hypertension, mitral- tricuspid- and pulmonic valvular disease. On multivariate analysis, higher RV diastolic pressure and etiology for RV dysfunction other than LHF were both associated with CH. Low cardiac output was associated with CH only amongst those without LHF.ConclusionsCH is most often seen in subjects with elevated RV diastolic pressure suggesting a congestive cause in most cases. CH associated with low cardiac output in patients without LHF suggests that low flow may be contributing to the patophysiology in some cases.
Background: Alterations in left ventricular (LV) twist (torsion) and untwist have been described for a variety of physiologic and pathologic conditions. Little information is available regarding changes in these parameters during normal pregnancy. Hypothesis: Pregnancy is associated with significant changes in LV torsional mechanics. Methods: Left ventricular twist and untwist was measured in 32 pregnant females (mean gestation 199 ± 48 d) and 23 nonpregnant controls using speckle-tracking echocardiography.Results: Left ventricular ejection fraction (68 ± 5% vs 66 ± 5%) was similar between the groups (P not significant). There was a significant increase in peak LV twist from nonpregnant controls (9.4 ± 3.7 degrees) to second-trimester (12.0 ± 4.2 degrees) and third-trimester subjects (12.6 ± 5.9 degrees, all P < 0.05). Peak LV twist velocity was also increased in second-and third-trimester groups compared with controls (94 ± 24 degrees/sec and 93 ± 30 vs 64 ± 21 degrees/sec, respectively, both P < 0.05). Both peak untwist velocity and time to peak untwist velocity were not significantly different between groups (P not significant). Multiple regression analysis indicate that only systolic blood pressure (r = 0.394, P = 0.005) was an independent predictor for increased LV torsion. Conclusions: There are significant changes in LV torsional indices during the course of pregnancy, whereas untwist parameters remain unchanged. Blood pressure is independently associated with increased torsion during pregnancy.
IntroductionPregnancy is associated with reversible adaptations in maternal systolic and diastolic left ventricular (LV) function. 1,2 Prior studies have shown increased preload and cardiac output, 3 -5 decreased systemic vascular resistance, 2,6 and increased LV mass and wall thickness 7 during pregnancy. Changes in LV fractional shortening are less well-defined, with the literature offering conflicting data. 8 -10 Little information is available concerning alterations in LV torsion (LV Tor ), the helical twisting motion of the LV about its longitudinal long axis. 11 Speckle-tracking echocardiography (STE) is a noninvasive method that allows for rapid, objective quantification of LV Tor . 12 Numerous studies have demonstrated that STE can accurately quantify differences in LV Tor associated with various pathophysiologic conditions. 13 -16 We used STE to measure LV Tor in healthy pregnant women and nonpregnant controls.
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