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.
Acute myocardial infarction (AMI) occurs when there is evidence of myocardial injury (an increase in cardiac troponin values) and clinical evidence of myocardial ischemia. Data from the Jakarta Acute Coronary Syndrome Registry states that in 2014 there were 3015 patients with acute coronary syndrome (ACS); half of them were diagnosed with ST Elevation Myocardial Infarction (STEMI). Among patients with STEMI, 46% of cases did not receive reperfusion therapy. This case report aimed to describe the features, complications and management of ST segment elevation with left ventricular thrombus. A 44-year-old male patient came with complaints of chest pain that had been experienced for 8 h before entering hospital. The chest pain did not decrease with rest and radiated to the back of the chest. The patient is a heavy smoker and during electrocardiographic examination, ST elevation was found in leads V1-4. It was decided to perform primary percutaneous coronary intervention, but failed due to administrative matters. The patient, therefore, received Loading Aspilet 160 mg chewable, loading Ticagrelor 180 mg orally, Isosorbide dinitrate 5 mg Sublingual, repeated up to 3 times every 5 min, Glyceryl trinitrate 2 × 5 mg orally, Morphine 2 mg intravenously (after isosorbide dinitrate does not respond), Bisoprolol 1 × 2.5 mg orally, Atorvastatin 1 × 40 mg orally, Laxadyn syrup 3 × 10cc orally, Fibrinolytic with streptokinase 1.5 million units intravenous drip then followed by Injection enoxaparin 0.6 cc/12 h (for 5 days). After administering a streptokinase injection, a repeat electrocardiographic examination was performed and found a decrease in ST elevation in leads V1-4. Clinically, the chest pain began to decrease. The patient underwent echocardiography for the first time on
Coronary microvascular dysfunction (DMK) is a condition of patients who are accompanied by complaints of chest pain where the results of coronary angiography examination are normal and this is almost 49% with 60% of patients diagnosed with DMK. Another study said that about 40% of patients with DMK showed coronary flow reserve (CFR <2) of about 40% and the WISE study (Women's Ischaemia Syndrome Evaluation) showed that about 47% of patients with chest pain had normal coronary arteries. DMK can be divided into 4 groups; DMK with no coronary arterial disease (CAD) obstruction and myocardial disease, DMK with myocardial disease where this occurs due to remodeling of intramural coronary arteries, DMK with CAD (coronary arterial disease) or acute myocardial infarction with or without ST segment, iatrogenic typhoid DMK occurs after coronary recanalization caused by vasoconstriction and distal embolization. The mechanism of action of DMK can be caused by several factors, namely endothelial dysfunction, smooth muscle dysfunction, decreased diastolic perfusion time, damage to blood vessels and damage to the vascular and microvascular remodeling. And to enforce this DMK, there are several tests carried out in diagnosing the disease, some of which are invasive and non-invasive so that by enforcing the diagnosis of this disease, treatment for DMK can be done immediately and optimally.
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