Background: Pregnant women with heart disease (HD) are at an increased risk for maternal and neonatal adverse events. However, the effect of pregnancy on clinical status and ventricular function in women with HD has not been examined in a controlled study.
Methods And Results: Ninety-three women with HD were studied longitudinally. Of these, fifty-three underwent clinical and echocardiographic evaluation before and 1.5+/-1.1 years after pregnancy (pregnancy group), whereas forty served as controls matched for age (28.6+/-4.6 versus 28.5+/-6.6, p=0.88), diagnosis, and length of follow-up (2.9+/-1.4 versus 2.6+/-1.1, p=0.23). NYHA functional class remained unchanged in both groups during follow-up. End diastolic and end systolic dimensions and shortening fraction of the morphologic left ventricle also remained unchanged. Furthermore, systemic and subpulmonary ventricular function remained unchanged in the pregnancy and control groups on semiquantitative analysis. Pregnancy, however, was associated with a persisting increase in subpulmonary ventricular size in patients with tetralogy of Fallot (ToF) which was not present in tetralogy controls. Furthermore, diagnosis of ToF was the only predictor of an increase in subpulmonary ventricular size after pregnancy on univariate logistic regression analysis (OR 8.8[95% CI 1.9-41.1], p=0.006).
Conclusions: In this longitudinal controlled study amongst women with HD no deleterious midterm effects of pregnancy on clinical status and right and left ventricular function were found. However, pregnancy was associated with a persisting increase in subpulmonary ventricular size, attributable to patients with repaired ToF. This may have prognostic implications and merits further investigation.
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http://dx.doi.org/10.1016/j.ijcard.2008.09.001 | DOI Listing |
Sci Rep
January 2025
Division of Cardiology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Myocyte disarray and fibrosis are underlying pathologies of hypertrophic cardiomyopathy (HCM) caused by genetic mutations. However, the extent of their contributions has not been extensively evaluated. In this study, we investigated the effects of genetic mutations on myofiber function and fibrosis patterns in HCM.
View Article and Find Full Text PDFCardiooncology
January 2025
ProCardio Center for Innovation, Department of Cardiology, Oslo University Hospital, Oslo, Norway.
Background: Although anthracycline-related cardiotoxicity is widely studied, only a limited number of echocardiographic studies have assessed cardiac function in breast cancer survivors (BCSs) beyond ten years from anthracycline treatment, and the knowledge of long-term cardiorespiratory fitness (CRF) in this population is scarce. This study aimed to compare CRF assessed as peak oxygen uptake (V̇O), cardiac morphology and function, and cardiovascular (CV) risk factors between long-term BCSs treated with anthracyclines and controls with no history of cancer.
Methods: The CAUSE (Cardiovascular Survivors Exercise) trial included 140 BCSs recruited through the Cancer Registry of Norway, who were diagnosed with breast cancer stage II to III between 2008 and 2012 and had received treatment with epirubicin, and 69 similarly aged activity level-matched controls.
Clin Neurol Neurosurg
December 2024
Department of Anatomy, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India. Electronic address:
Background: The complex structure and function of the cerebrum make it a key focus in neuroscience research. It develops from telencephalic vesicles through processes such as cell growth, division, and migration from the neuroepithelium's ventricular matrix, forming the six-layered isocortex or neocortex. Multipotent neuroepithelial cells give rise to both neuronal and glial precursors, which populate the cerebral cortex.
View Article and Find Full Text PDFCurr Vasc Pharmacol
January 2025
Department of Cardiology, Athens University School of Medicine, Athens, Greece.
Introduction/objective: Atrial fibrillation (AF) could present with slow ventricular-response; bradycardia could facilitate the emergence of AF. The conviction that one "does not succumb" from bradycardia as an escape rhythm will emerge unless one sustains a fatal injury following syncope is in stark difference with ventricular tachyarrhythmia (VA), which may promptly cause cardiac arrest. However, this is not always the case, as a life-threatening situation may emerge during the bradycardic episode, i.
View Article and Find Full Text PDFJ Physiol
January 2025
Center for Developmental Health, Oregon Health & Science University, Portland, OR, USA.
Robust preclinical models of asymmetric ventricular loading in late gestation reflecting conditions such as hypoplastic left heart syndrome are lacking. We characterized the morphometry and microvascular function of the hypoplastic left ventricle (LV) and remaining right ventricle (RV) in a sham-controlled late gestation fetal lamb model of impaired left ventricular inflow (ILVI). Singleton fetuses were instrumented at ∼120 days gestational age (dGA; term is ∼147 days) with vascular catheters, an aortic flow probe and a deflated left atrial balloon.
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