Cyrus Hadadi is a first-year cardiology fellow at Geisinger Medical Center in Danville, Pennsylvania. He graduated from the University of Maryland, College Park and received a medical degree from Drexel University College of Medicine in Philadelphia, Pennsylvania. He completed his residency in internal medicine at the University of Maryland Medical Center in Baltimore, Maryland.
Coronary artery spasm is an important factor in the pathogenesis of ischemic heart disease. Ischemic episodes caused by coronary spasm may induce arrhythmia, including cardiac arrest. A 53-year old male smoker presented after witnessed cardiac arrest. He was in ventricular fibrillation and underwent successful defibrillation. On arrival to the emergency department he had ST elevations in the anterolateral ECG leads V2 – V6. The patient was treated for ST-elevation myocardial infarction (STEMI) with heparin, amiodarone, aspirin and clopidogrel. Laboratory testing was significant for cardiac Troponin I peak at 6.25 ng/mL. Urine toxicology was negative. Echocardiogram revealed decreased left ventricular ejection fraction of 30% with an akinetic anteroseptum and apex. Coronary angiography revealed no significant disease of the left anterior descending (LAD) coronary artery. After repeat injection of dye, the LAD developed complete occlusion concerning for coronary artery spasm that was associated with tachycardia to 178 beats per minute and severe hypertension to 200/133 mmHg. The spasm and associated symptoms resolved with intracoronary nitroglycerin administration. This patient presented with STEMI in the absence of obstructive coronary artery disease. Coronary angiography images confirmed that the patient’s symptoms were induced by spasm of the LAD. Potential mechanisms of coronary spasm include endothelial dysfunction and vascular smooth muscle cell hyperreactivity. In the setting of active cardiac catheterization, intracoronary nitrates and atropine have been demonstrated to reverse coronary spasm. Outpatient treatment options include calcium channel blockers and long-acting nitrates, as well as magnesium, statins, antioxidants, angiotensin antagonists and anti-inflammatories.
The objectives are to study the blood flow conditions by the MRI and CT.rnIn 17 healthy volunteer (18-52y) at the different sites of the aorta peak velocity, net flow and flow acceleration has been investigated. rnAt the outer curvature of the aorta in the end systole flow separates. At the isthmus, flow acceleration in the initial diastole is 8.7 times higher than that in systole. Net flow from systole to diastole increases 2.5± 0.5 folds. From the end systole to the initial diastole there is a plateau on the net flow graph. At the outer curvature of isthmus, group waves at the boundary reflection, changes in phase at 1800 at the oscillation - 0.8Hz and 1.6Hz. Blood density from the aortic isthmus, to the abdominal aorta equals to - 51±3H to 31± 4H respectively. Blood motion at the boundary layer forms the surface wave. At the outer wall isthmus of the aorta, pulse pressure at the reflection is in resonance with the end systolic pressure drop and amplitude of the wall stress increases. At the end systole at the outer wall, wave packets with the different frequencies are formed. Erythrocyte aggregation at the ejection, facilitates to the energy high efficiency transmission from the heart, to the blood. Wave frequency dispersion destroy the flow cell aggregates, whereas at the wall reflection and cyclic loading it shears the endothelial sheet.