Influence of socioeconomic factors on pregnancy outcome in women with structural heart disease

OBJECTIVE: Cardiac disease is the leading cause of indirect maternal mortality. The aim of this study was to analyse to what extent socioeconomic factors influence the outcome of pregnancy in women with heart disease.  METHODS: The Registry of Pregnancy and Cardiac disease is a global prospective registry. For this analysis, countries that enrolled ≥10 patients were included. A combined cardiac endpoint included maternal cardiac death, arrhythmia requiring treatment, heart failure, thromboembolic event, aortic dissection, endocarditis, acute coronary syndrome, hospitalisation for cardiac reason or intervention. Associations between patient characteristics, country characteristics (income inequality expressed as Gini coefficient, health expenditure, schooling, gross domestic product, birth rate and hospital beds) and cardiac endpoints were checked in a three-level model (patient-centre-country).  RESULTS: A total of 30 countries enrolled 2924 patients from 89 centres. At least one endpoint occurred in 645 women (22.1%). Maternal age, New York Heart Association classification and modified WHO risk classification were associated with the combined endpoint and explained 37% of variance in outcome. Gini coefficient and country-specific birth rate explained an additional 4%. There were large differences between the individual countries, but the need for multilevel modelling to account for these differences disappeared after adjustment for patient characteristics, Gini and country-specific birth rate.  CONCLUSION: While there are definite interregional differences in pregnancy outcome in women with cardiac disease, these differences seem to be mainly driven by individual patient characteristics. Adjustment for country characteristics refined the results to a limited extent, but maternal condition seems to be the main determinant of outcome

Comparison of Candesartan Versus Metoprolol for Treatment of Systemic Hypertension After Repaired Aortic Coarctation

Even after successful repair, hypertension is one of the main determinants of cardiovascular morbidity and mortality in patients with aortic coarctation (CoA). We compared the effect of candesartan (angiotensin 11 receptor blockade) and metoprolol (beta-adrenergic receptor blockade) on blood pressure, large artery stiffness, and neurohormonal status in hypertensive patients after repair of CoA. In the present open-label, crossover study, hypertensive patients after CoA repair were first randomly assigned to treatment with candesartan 8 mg or metoprolol 100 mg once per day. After 8 weeks of treatment with one of the drugs, the other treatment was given for 8 weeks. The treatment effects were assessed with 24-hour ambulatory blood pressure monitoring, measurement of large artery stiffness, and neurohormonal plasma levels at baseline and after 8 weeks of either treatment. Sixteen patients (mean age 37 +/- 12 years, 26 +/- 15 years after repair, 63% men) completed the study. The 24-hour mean arterial pressure at baseline was 97.7 +/- 6.2 mm Hg. Metoprolol (mean dose 163 +/- 50 mg/day) decreased the mean arterial pressure (7.0 +/- 4.2 and 4.1 +/- 3.6 mm Hg, respectively) more than did candesartan (mean dose 13 +/- 4 mg/day; p = 0.018, 95% confidence interval 0.6 to 5.5). Large artery stiffness did not change with either treatment. With metoprolol, plasma B-type natriuretic peptide increased and plasma renin decreased. With candesartan, the plasma renin and noradrenaline levels increased and aldosterone levels decreased. In conclusion, in adult hypertensive patients after CoA repair, metoprolol had more of an antihypertensive effect than did candesartan. Moreover, the neurohormonal outcome did not support a significant role for the renin-angiotensin system in the causative mechanism of hypertension after CoA. (C) 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;105:217-222

Hemodynamic adaptation to pregnancy in women with structural heart disease

Background: Many women with structural heart disease reach reproductive age and contemplate motherhood. Pregnancy induces and requires major hemodynamic changes. Pregnant women with structural heart disease may have a reduced cardiac reserve. There are no longitudinal data on cardiovascular adaptation throughout pregnancy in women with structural heart disease. Methods: Thirty-five women with structural heart disease were included in a prospective observational trial. Maternal hemodynamics were assessed before conception, during pregnancy and 6 months postpartum by transthoracic echocardiography. Uteroplacental perfusion was analyzed by obstetric Dopplers. Longitudinal evolution over time was analyzed as well as the long term influence of pregnancy on cardiac function. Results: Cardiac output (CO), stroke volume (SV), left ventricular mass (LV mass) and E/E' ratio significantly increased and ejection fraction (EF) and fractional shortening (FS) decreased during pregnancy. There was a statistically significant difference in EF, FS and E/E' ratio before and after pregnancy. Conclusions: The characteristic pattern of hemodynamic adaptation to pregnancy is attenuated in women with structural heart disease. The pregnancy related volume load induces progression of diastolic dysfunction. Our data suggest a persistent reduction in systolic and diastolic cardiac functions after pregnancy in women with structural heart disease. (c) 2012 Elsevier Ireland Ltd. All rights reserved

Late cardiac remodeling after primary percutaneous coronary intervention-five-year cardiac magnetic resonance imaging follow-up.

BACKGROUND: Primary percutaneous coronary intervention (PPCI) preserves function and improves survival. The late effects of PPCI on left ventricular remodeling, however, have not yet been investigated on cardiac magnetic resonance imaging (CMRI). METHODS AND RESULTS: Twenty-five patients with acute myocardial infarction (AMI) treated with PPCI underwent CMRI within 10 days, at 4 months and at 5 years. Left ventricular ejection fraction (LVEF), end-diastolic volume (EDV) and end-systolic volume were quantified on cine images. Infarct mass and transmural extent of infarction were quantified on contrast-enhanced imaging. In all patients EDV increased significantly in the early phase (192 \ub1 40 ml to 211 \ub1 49 ml, P 64 0.01) and LVEF improved significantly (42 \ub1 9% to 46 \ub1 9%, P=0.02). In the late phase (>4 months) no significant changes were observed (LVEF 44 \ub1 9%, P=0.07; EDV 216 \ub1 68 ml, P=0.38). Three different groups could be identified. One-third (32%) had no dilatation at all; one-third (32%) had limited dilatation at 4 months without progression later; and 36% had progressive dilatation both at 4 months and at late follow-up. This third group had an average increase in EDV of 20% in the acute phase followed by an additional 13%. The strongest predictor for progressive dilatation was infarct mass. CONCLUSIONS: Even in the era of PPCI for AMI followed by optimal medical therapy, one-third of patients had progressive dilatation, which was best predicted by infarct mass

Hemodynamic adaptation to pregnancy in women with structural heart disease.

BACKGROUND: Many women with structural heart disease reach reproductive age and contemplate motherhood. Pregnancy induces and requires major hemodynamic changes. Pregnant women with structural heart disease may have a reduced cardiac reserve. There are no longitudinal data on cardiovascular adaptation throughout pregnancy in women with structural heart disease. METHODS: Thirty-five women with structural heart disease were included in a prospective observational trial. Maternal hemodynamics were assessed before conception, during pregnancy and 6 months postpartum by transthoracic echocardiography. Uteroplacental perfusion was analyzed by obstetric Dopplers. Longitudinal evolution over time was analyzed as well as the long term influence of pregnancy on cardiac function. RESULTS: Cardiac output (CO), stroke volume (SV), left ventricular mass (LV mass) and E/E' ratio significantly increased and ejection fraction (EF) and fractional shortening (FS) decreased during pregnancy. There was a statistically significant difference in EF, FS and E/E' ratio before and after pregnancy. CONCLUSIONS: The characteristic pattern of hemodynamic adaptation to pregnancy is attenuated in women with structural heart disease. The pregnancy related volume load induces progression of diastolic dysfunction. Our data suggest a persistent reduction in systolic and diastolic cardiac functions after pregnancy in women with structural heart disease

Late cardiac remodeling after primary percutaneous coronary intervention: Five-year cardiac magnetic r

Background: Primary percutaneous coronary intervention (PPCI) preserves function and improves survival. The late effects of PPCI on left ventricular remodeling, however, have not yet been investigated on cardiac magnetic resonance imaging (CMRI). Methods and Results: Twenty-five patients with acute myocardial infarction (AMI) treated with PPCI underwent CMRI within 10 days, at 4 months and at 5 years. Left ventricular ejection fraction (LVEF), end-diastolic volume (EDV) and end-systolic volume were quantified on cine images. Infarct mass and transmural extent of infarction were quantified on contrast-enhanced imaging. In all patients EDV increased significantly in the early phase (192±40ml to 211±49ml, P≤0.01) and LVEF improved significantly (42±9% to 46±9%, P=0.02). In the late phase (>4 months) no significant changes were observed (LVEF 44±9%, P=0.07; EDV 216±68ml, P=0.38). Three different groups could be identified. One-third (32%) had no dilatation at all; one-third (32%) had limited dilatation at 4 months without progression later; and 36% had progressive dilatation both at 4 months and at late follow-up. This third group had an average increase in EDV of 20% in the acute phase followed by an additional 13%. The strongest predictor for progressive dilatation was infarct mass. Conclusions: Even in the era of PPCI for AMI followed by optimal medical therapy, one-third of patients had progressive dilatation, which was best predicted by infarct mass.   (Circ J 2013; 77: 81–88