Prosthetic valve obstruction (PVO) is a rare but feared complication of mechanical valve replacement. Diagnostic evaluation should focus on differentiating prosthetic valve thrombosis (PVT) from pannus formation, as their treatment options differ. History of sub-optimal anti-coagulation and post-op time course to development of PVO are useful clinical characteristics in differentiating thrombus from pannus formation. Treatment of PVT is influenced by the patient's symptoms, valve location, degree of obstruction and thrombus size and may include thrombolysis or surgical intervention. Alternatively, pannus formation requires surgical intervention. The purpose of this article is to review the pathophysiology, epidemiology, diagnostic approach and treatment options for aortic and mitral valve PVO.
A n 87-year-old man with a history of coronary artery disease, and having had 1-vessel coronary artery bypass surgery 10 years prior to admission, was admitted in a severe coma to the cardiovascular intensive care unit (CCU) for an acute myocardial infarction complicated by cardiogenic shock. He was intubated and started on inotropic and vasopressor support along with insertion of an intra-aortic balloon pump. Cardiac catheterization revealed 90% stenosis of the proximal left anterior descending artery, and a drug-eluting stent was implanted. However, he remained comatose and dependent on mechanical circulatory support. He rapidly developed acute kidney injury, requiring initiation of continuous venovenous hemodialysis. On the fourth hospital day, the family reported that the patient had stated on multiple occasions that he would not want to undergo aggressive diagnostic and treatment modalities if he was very sick and the prognosis was grim. The family requested to withdraw invasive and aggressive means of care. All life-sustaining measures were stopped, including inotropes/vasopressors, enteral feedings, the intraaortic balloon pump, and continuous venovenous hemodialysis. He was provided with pain medication (for pain/dyspnea) and sedatives (for distress), with subsequent extubation. A few hours later, he peacefully passed away. In this case, intensive care was withdrawn at the family's request. The team and family agreed that this course of action best honored the patient's wishes. It is sometimes painful to us, as physicians, to admit that our interventions do nothing else but prolong patient suffering. We often encounter situations like this during our fellowship training, especially in the CCU, where we deal with sick and complex patients who also have complicated end-of-life issues; thus, the following are some skills that we should seek to master to effectively and compassionately care for our terminal patients. 1. Prognostication. Prognostication, along with diagnosis and treatment, is a traditional core clinical skill of every physician (1) and should be part of every clinical encounter. For example, we now know that mortality rates among patients who develop refractory cardiogenic shock range from 50% to 80% and that only one-half of the patients with refractory heart failure who receive mechanical circulatory support survive to hospital discharge (2). However, in patients with compensated advanced heart failure, this is difficult to predict, because unlike many cancers that are characterized by a steep linear decline in performance status during the last few months of life, heart failure is characterized by unpredictable decompensations and improvements, with a subtler decline over time (3). Hyponatremia, hypotension, decline in functional status, and cachexia are associated with an increased mortality risk. Therefore, we should seek to develop a treatment plan but also formulate an individualized prognosis for each of our patients. 2.Communication. Most of the time, we avoid telling the patient that...
Coronary artery spasm has been reported during adenosine stress testing. Herein, we describe a transient ST-segment elevation following adenosine therapy for supraventricular tachycardia. A 38-year-old male presented to the emergency department with palpitations. Electrocardiogram showed supraventricular tachycardia with short RP interval. Vagal maneuvers were unsuccessful. Adenosine was then administered in two successive injections of 6 and 12 mg dosages, respectively. A subsequent 12-lead electrocardiogram revealed ST-segment elevation in inferior leads with reciprocal changes. Coronary angiography disclosed nonobstructive coronary disease. A postprocedure electrocardiogram exhibited normal sinus rhythm with nonspecific T wave abnormalities. Cardiac biomarkers were elevated with a peak troponin I of 0.32. Echocardiogram depicted bicuspid aortic valve and normal systolic function. Electrophysiological study revealed a concealed left accessory pathway and successful radiofrequency ablation was performed. Given the dynamic changes in the electrocardiogram, we hypothesize that this event was most likely a coronary vasospasm. The mechanism of coronary spasm following adenosine injection remains uncertain. Potential mediators include KATP channels and adenosine-2 receptors.
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