Incidence and predictors of atrial fibrillation after aortic repairs.
The incidence of atrial fibrillation and the clinical predictors for its development were studied in 153 patients who underwent thoracic and abdominal aortic repair.
Biomedical subjects
Publications and source records attributed to Ramdas G Pai.
The incidence of atrial fibrillation and the clinical predictors for its development were studied in 153 patients who underwent thoracic and abdominal aortic repair.
A survey conducted in a relatively homogeneous group of 527 Konkani subjects revealed a high prevalence of coronary artery disease (CAD) despite a lack of smoking and significant obesity. Traditional risk factors (age, gender, high cholesterol, hypertension, and diabetes) were significant predictors of CAD. In addition, duration of residence in the United States (US) emerged as a new independent risk factor. Independent predictors of CAD included age, gender, ever smoking, and duration of residence in the US. We conclude that acculturation may be a major risk factor for CAD in immigrant populations.
BACKGROUND AND OBJECTIVES: The mitral A wave is transmitted to the left ventricular (LV) outflow tract where it is registered as Ar wave. We have related its transit time to the LV late diastolic stiffness. We also observed incidentally that the duration of the transmitted Ar wave exhibited marked variability and hence investigated its hemodynamic correlates. METHODS AND RESULTS: Mitral A wave and the Ar wave in the LV outflow tract were recorded using pulsed wave Doppler technique simultaneous with high fidelity LV pressure recordings in 20 patients undergoing cardiac catheterization. A high-speed contrast left ventriculogram was obtained as well. The duration of both these wave forms were measured and A wave duration minus the Ar wave duration was measured. The A minus Ar wave duration (range 0-95 ms) correlated with LV end-diastolic pressure (r = 0.54, P = 0.014, range 4-32 mmHg), LV late diastolic stiffness (r = 0.62, P = 0.004, range 0.1-1.6 mmHg/ml) and the amount of LV pressure rise with atrial contraction (r = 0.67, P = 0.001, range 2-13 mmHg). CONCLUSION: A minus Ar wave duration is an easily obtainable Doppler parameter that is related to LV late diastolic filling pressures and stiffness and gives insights into aspects of LV diastolic function.
BACKGROUND: Patients with congestive heart failure have an annual mortality of 10% to 20% depending on disease severity. Though one third of these patients have normal left ventricular (LV) ejection fraction (EF), their natural history is poorly defined. Small population-based studies have suggested a more benign prognosis for patients with preserved LVEF. However, prognosis in hospitalized patients, who form a higher risk group, is not known. METHODS: We investigated the survival patterns of 2,258 patients with a primary hospital discharge diagnosis of congestive heart failure between 1990 and 1999. Survival was analyzed and patients with normal and reduced LVEF were compared. RESULTS: Their age was 71 +/- 11 years, and 97% were men. There were 1,535 deaths over a mean follow up of 786 days. Of these, 963 (43%) patients had a normal LVEF (>/=55%). Patients with normal LVEF were of the same age as those with reduced LVEF, but had a lower prevalence of atrial fibrillation (20 versus 26%, P =.03), left bundle branch block (2 versus 12%, P <.0001), significant mitral regurgitation (5 versus 31%, P <.0001) and electrocardiographic evidence of myocardial infarction (38 versus 60%, P <.0001). Despite lesser comorbidities, they had a higher mortality hazard, with a 5-year survival of 22% compared with 28% for those with systolic heart failure (P =.007). Proportional hazards model showed presence of normal EF as a categoric variable to be an independent predictor of mortality in those with heart failure after correcting for age and rhythm. CONCLUSIONS: Prognosis of hospitalized patients with congestive heart failure and normal LVEF is worse than those with reduced EF despite lesser comorbidities. Studies addressing optimal management of these patients are warranted.
BACKGROUND: Increased QT interval and QT dispersion have been associated with higher mortality in population-based studies and in patients with myocardial infarction. However, the prognostic significance of these measurements in patients with left ventricular (LV) systolic dysfunction is not clear. METHODS AND RESULTS: Rate corrected QT interval (QTc) and QT dispersion (QTd) were measured by means of an automated method from digitized echocardiograms in 2265 patients with an LV ejection fraction < or =40% and were related to survival. Increased QTc was strongly related to mortality in the whole group and in subsets on the basis of age and the level of LV systolic dysfunction. There was a graded increase in mortality rate with an increase in QTc. The effect of QTc on mortality was incremental to the effects of age and ejection fraction. QT interval was measurable in > or =6 leads in 1193 patients in whom QTd was computed. QTd higher than the mean value of 35 ms was associated with an increase in all cause mortality (P =.04). Its mortality impact was most pronounced in the older patients, patients with more severe LV dysfunction, and patients with increased QTc. CONCLUSIONS: Both QTc prolongation and increased QTd are associated with higher mortality rate in patients with moderate and severe LV dysfunction.
We present a case of a patient who was pregnant and had symptomatic, intermittent obstruction of her St Jude mitral prosthesis showing a very unique Doppler flow pattern suggesting impaired disk movement with every other cardiac cycle. Mechanism of this "obstruction alternans" is discussed.
BACKGROUND AND AIMS OF THE STUDY: The mitral annulus shows dynamic changes in shape and size during the cardiac cycle. A smaller size in end-diastole is attributed to the sphincteric action of atrial systole, and this may be important for functional integrity of the mitral valve. However, the effect of atrial fibrillation (AF) on dynamic changes in mitral annular size in humans is not known. METHODS: Mitral annular diameters in apical four- and two-chamber views were measured using echocardiography in 25 patients in atrial fibrillation, and in 37 subjects in normal sinus rhythm at mid-diastole, end-diastole and end-systole. Mitral annular area was computed assuming elliptical geometry. RESULTS: Patients in sinus rhythm showed a significant increase in mitral annular area of 25.9 +/- 12.8% with ventricular systole compared to its area in end-diastole (p < 0.0001), and a 10.5 +/- 8.4% reduction with atrial systole compared to mid-diastole (p < 0.001). Patients in AF had larger mitral annuli which showed non-significant changes in size between these three phases of the cardiac cycle. Percent reduction in mitral annular area in the latter half of diastole correlated significantly with left atrial (LA) diameter (r = -0.54, p < 0.0001), LA volume (r = -0.50, p < 0.0001), left ventricular (LV) fractional shortening (r = 0.37, p = 0.0036), mitral annular area in mid-diastole (r = -0.41, p = 0.0011) and mitral annular area in end-diastole (r = -0.64, p < 0.0001). That is, atrial sphincteric action on the mitral annulus was less in the presence of larger left atrium or the mitral annulus. Stepwise multiple regression analysis showed rhythm and mitral annular size to be independent predictors of dynamic changes in mitral annular area. CONCLUSION: It is concluded that AF blunts or eliminates the phasic changes in mitral annular size during the cardiac cycle with loss of its presystolic sphincteric action; this may have implications in the genesis and surgical correction of mitral regurgitation.
BACKGROUND AND AIM OF THE STUDY: Mitral regurgitation (MR) is frequent in patients with severe calcific aortic stenosis (AS). This complicates not only the clinical course of AS, but also its surgical management. The aim of the present study was to investigate the mechanism of genesis of MR in patients with severe AS. METHODS: The echocardiographic database was searched for subjects with severe AS defined as a calculated (continuity equation) aortic valve area < 0.7 cm2. Patients with previous valve surgery were excluded; thus, the study group comprised 123 patients. RESULTS: Among 123 patients (mean age 75 +/- 10 years) with severe AS, 54 (44%) had no MR, 37 (30%) had mild MR, 20 (16%) had moderate MR, and 12 (10%) had severe MR. Hence, moderate or severe MR was present in approximately 25% of patients. Patients with moderate or severe MR had a larger left ventricular (LV) end-diastolic diameter (5.1 +/- 1.0 versus 4.8 +/- 0.8 cm; p = 0.08), larger LV end-systolic diameter (3.8 +/- 1.2 versus 3.1 +/- 0.8 cm; p = 0.001), lower LV ejection fraction (40 +/- 16 versus 58 +/- 18%; p = 0.0001), higher degree of aortic regurgitation (p = 0.002), larger left atrial diameter (4.7 +/- 0.9 versus 4.1 +/- 0.6 cm; p = 0.001), lower LV free wall thickness (1.1 +/- 0.2 versus 1.3 +/- 0.4 cm; p = 0.05), and lower combined wall thickness (2.4 +/- 0.3 versus 2.7 +/- 0.5 cm; p = 0.02) and relative wall thickness (0.5 +/- 0.1 versus 0.6 +/- 0.1 cm; p = 0.02). Both groups had similar degrees of AS and mitral annular calcification. CONCLUSION: MR in severe AS is associated with a larger LV size and lesser wall thickness, and this may result from failure of adequate adaptive LV hypertrophy necessitated by the pressure overload imposed by AS. This might have important clinical implications in terms of timing of aortic valve replacement before the left ventricle begins to dilate, and also in the choice of pharmacologic therapy that may modulate the adaptive response of the left ventricle.
Cardiac echinococcosis is a rare condition, and its manifestations are protean depending upon its site of infestation. We report a case of hydatid heart disease presenting like an acute cardiac ischemic episode associated with a rise in serum cardiac enzymes secondary to left ventricular free wall dissection caused by ruptured intramyocardial echinococcal cyst. The resultant complex cardiac anatomy was characterized fully by echocardiographic examination.
Increased QT interval and QT dispersion have been associated with increased mortality in a variety of cardiovascular disorders including heart failure. However, the biological correlates of these abnormalities are not clear. QTc and QTd were measured in an automated fashion from digitized electrocardiograms in 2,265 patients with an LV ejection fraction </=40% and were related to clinical, electrocardiographic, and echocardiographic variables. The QTc interval increased with increasing age (P =.0003), heart rate (P <.0001), LV dimensions (P <.0001), left atrial diameter (P <.0001), estimated right atrial pressure (P <.0001), QRS duration (P <.0001), bundle branch blocks (P <.0001) and degree of mitral and tricuspid regurgitation (P <.0001) and decreasing LV ejection fraction (P <.0001) QT dispersion increased with increasing LV isovolumic relaxation time (P =.004) and QTc (P <.0001) and decreased with faster heart rate (P <.0001) and higher right atrial pressure (P =.0007). The biological relationships of QTc and QTd warrant further investigations.
Growing evidence suggests that atherosclerosis is an immune-mediated inflammatory process and that cytokines participate as mediators in this process. Of the cytokines, interleukins, which are released from both immune and nonimmune cells of vascular wall, are found to have multiple effects. Interleukin-2 (IL-2), a cytokine produced by activated T-lymphocytes, has been found to further activate the T cells and may potentially enhance atherogenesis. Apo-E-deficient mice fed with atherogenic diet were injected intraperitoneally twice a week with placebo, IL-2, or anti-IL-2 antibody for a period of 6 weeks. Group 1 (n = 6) was injected with bovine serum albumin (BSA) in phosphate-buffered saline (PBS) and served as controls. Group 2 (n=6) was injected with 2 x 10(4) units of recombinant murine IL-2 (rmIL-2) per dose reconstituted with BSA in PBS. Group 3 (n=6) was injected with 5 microg of anti-IL-2 per dose reconstituted with BSA in PBS. Aortic sections were analyzed and atherosclerotic burden was quantified. Compared to controls, injection of IL-2 increased measures of atherosclerosis such as the average lesion score (10.7 +/-0.5 vs 9.3 +/-1.1, p=0.04) and the lesion size as a fraction of aortic area (0.51 +/-0.03 vs 0.41 +/-0.05, p=0.01). Injection of anti-IL-2 had a profound antiatherogenic effect. It significantly reduced the average number of lesions per cross section (2.6 +/-0.6 vs 4.3 +/-0.6, p=0.03), the average lesion score (4.6 +/-1.9 vs 9.3 +/-1.1, p=0.02), the lesion area/circumference (0.35 +/-0.08 vs 0.62 +/-0.10, p=0.007), and the lesion size/aortic area (0.23 +/-0.07 vs 0.41 +/-0.05, p=0.03). These results indicate that IL-2 is an atherogenic cytokine in apo-E-deficient mice and anti-IL-2 is protective against atherosclerosis. This may have important clinical implications in modifying the atherosclerotic process.