The phenomenon of angina chest pain without significant epicardial coronary artery stenosis, but accompanied by a slowdown in coronary blood flow is often found in patients with symptoms of acute coronary syndrome who undergoing invasive coronary angiography. This phenomenon of slow coronary blood flow is then called the coronary slow flow phenomenon (CSFP). The pathogenesis mechanism of CSFP remains unclear. The pathogenesis of CSFP is thought to be multifactorial. Endothelial dysfunction, small vessel disease, inflammation, renin system angiotensin aldosterone, atherosclerosis are thought to be involved in the pathogenesis of CSFP. Cardiovascular disease incidence and death were associated with elevated levels of Fibroblast growth factor-23 (FGF-23). High levels of FGF-23 can lead to formation of blood vessel calcification, left ventricular hypertrophy, arterial stiffness, endothelial dysfunction, increased inflammatory markers and elevated levels of angiotensin II. It is suspected that FGF-23 has a role in this event other than as a regulator of bone and mineral metabolism. This literature review aims to determine the relationship between fibroblast growth factor-23 and the pathophysiology of CSFP. Based on the broad role of FGF-23, it is possible that FGF-23 is involved in the pathogenesis of CSFP.
Atrial septal defect (ASD) is the most common form of congenital heart disease. Left-to-right shunting leads to right ventricular (RV) volume overload with excessive pulmonary blood flow. In the absence of pulmonary hypertension, pregnancy is generally well tolerated in the setting of an ASD. This case report aimed to describe the features and the multidisciplinary approach management in secundum ASD, severe pulmonary hypertension in pregnancy. A 31 years old woman, pregnant with her second child at 35 weeks gestational age came with a primary complaint of increased shortness of breath a day before being admitted to the hospital. Three months before being admitted to the hospital she complained of shortness of breath when walking ± 20 m. The complaint was felt when her pregnancy was 23 weeks. The shortness of breath got worse with increasing gestational age. She suspected she had a heart problem. The first child was born in 2013, 33 weeks gestational age, spontaneously, weighing 1400 g. Specific examination revealed a pan systolic murmur, maximum punctum ICS 2-3 left parasternal, grade 5/6, spreading medially, wide fixed splitting S2. Echocardiography found right atrial dilatation, interatrial septal defect left to right shunt, severe tricuspid regurgitation, severe pulmonary hypertension, and ejection fraction 73%. The patient had pregnancy termination, right heart catheterization and surgical closure. The patient has clinical improvement without any complications. In conclusion, pregnancy remains contraindicated in patients with ASDs associated with severe pulmonary hypertension due to poor maternal and fetal outcomes. Cardiology follow up during pregnancy should be adapted to clinical symptoms. Pulmonary hypertension associated with an ASD is associated with high morbidity and mortality. Patients should be monitored closely and specialized by a multidisciplinary team approach to achieve optimum outcomes.
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