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UNLABELLED: Type A aortic dissection with concurrent ST-elevation myocardial infarction (STEMI) is relatively rare. However, it can be potentially fatal and easily misdiagnosed as STEMI alone. Misdiagnosis will lead to inappropriate administration of anticoagulant and thrombolytic therapy and delayed surgical repair of the aorta. In patients with STEMI, short reperfusion time is associated with improved survival, and minimizing the door-to-balloon time is the goal of therapy worldwide. However, signs critical for differential diagnosis may be overlooked in the rush to primary percutaneous coronary intervention. When a patient is encountered who presents with chest pain and ST elevation on electrocardiogram, STEMI should not be the only diagnosis considered. By using bedside available information, detailed history taking and focused physical examination, it is possible to avoid a mistaken diagnosis. Here we report a case of Stanford type A aortic dissection with STEMI that was initially misdiagnosed as sole acute inferior wall myocardial infarction. Patient mortality may have resulted from delayed diagnosis and surgical treatment. KEY WORDS: Acute myocardial infarction; Aortic dissection.
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Coronary artery spasm constitutes a significant portion of patients with acute coronary syndrome. Calcium channel blocker and nitrate are the mainstream therapies, but some patients are medically refractory to these medical therapies. In addition, the best treatment strategies for these patients remain uncertain, and medically refractory left main coronary artery spasm is a clinical dilemma. The present case report presents a 43-year-old man with such condition, which was successfully treated by percutaneous coronary intervention with implantation of a drug-eluting stent. He remained symptom-free for three years, without restenosis on follow-up angiography.
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Stress cardiomyopathy (SCM) is a syndrome of transient cardiac abnormalities precipitated by intense emotional or physical stress. Differentiating SCM from acute myocardial infarction is often difficult but vital to avoid subjecting SCM patients to unnecessary reperfusion therapy and invasive coronary angiography. For accurate diagnosis, it is important that physicians be familiar with the current diagnostic criteria, most susceptible populations, and typical triggers for SCM. SCM occurs almost exclusively in post-menopausal women, a group with a high frequency of psychiatric disorders. Thus, in addition to typical trigger events, comorbid psychiatric disorders may contribute to SCM onset. We report a rare case of recurrent SCM with distinct electrocardiographic abnormalities during each presentation in a post-menopausal woman with depression.
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Pacemaker implantation is associated with the potential for various acute and late complications. Though they rarely occur, massive pulmonary air embolisms are lethal. We report the case of a 72-year old male with sick sinus syndrome who underwent permanent pacemaker implantation. Sedation was administered due to back pain with the resultant appearance of snoring. The procedure was complicated with repeated massive pulmonary air embolisms. The events occurred after the leads had been placed in the sheaths. The patient was successfully resuscitated with fluid challenge, O(2) supplement, vasopressor and catheter aspiration. This case illustrates that in a heavily sedated, snoring patient, the marked negative intrathoracic pressure can overcome the frictional resistance of air to being sucked into the gap between the lead body and sheath's wall. Careful manipulation alone is not enough to prevent pulmonary air embolisms. Aggressive treatment for upper airway obstruction is important. The use of a sheath with a haemostatic valve is strongly recommended if the upper airway obstruction cannot be treated adequately.