Cardiac troponins are the most sensitive and specific markers of myocardial injury. In fact, the Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction (MI) states that troponins are the preferred cardiac marker for detecting myocardial injury. For the aforementioned reasons, troponin levels are routinely ordered for patients presenting to the emergency department with chest pain, dyspnea, syncope, or any other possible presentations of MI. While troponin levels do reflect the extent of myocardial damage, they do not necessarily indicate myocardial ischemia in a subset of patients. Elevated troponin levels can be due to a wide array of mechanisms in the absence of myocardial ischemia and injury. Thus, relying solely on troponin levels, in the presence of a normal electrocardiogram (ECG), to diagnose myocardial ischemia can lead to unnecessary and expensive invasive testing. It is therefore important for the clinician to keep in mind the varying causes of troponin elevations in order to provide the highest value care to the patient. We present a case and review of literature regarding patients who present with elevated troponin levels in the absence of any coronary artery disease.
Hürthle cell carcinoma (HCC) is a variant of a follicular carcinoma with a tendency to higher frequency of metastases and a lower survival rate. However, intracavitary cardiac metastases from thyroid HCC are extremely rare. We describe the case of a 57-year-old female with thyroid HCC, 5 years after total thyroidectomy, who presented with dyspnea associated with hypoxia and hypotension. The computed tomography angiogram showed extensive pulmonary embolism and a 6-cm right atrial mass while the lower-extremity deep vein thrombosis studies were negative. This patient received a cardiac thrombectomy using cardiopulmonary bypass support. However, intraoperatively, we found out that the mass was from the mediastinum, directly extending into the heart and clearly unresectable since it effaced at least 1/3 of the right atrial wall. The core biopsy of the mass confirmed that it was metastatic poorly differentiated HCC of thyroidal origin. The patient eventually died of respiratory failure due to a massive pulmonary embolism. For cancer patients with unexplained dyspnea, cardiac metastases should be considered regardless of anticoagulation prophylaxis, especially when there is no deep vein thrombosis in the lower limbs. Early recognition of intracavitary cardiac metastases may help in providing prompt treatment and improving the prognosis.
Previous studies using intracoronary electrocardiography have demonstrated that ST-T alternans can develop during standard balloon coronary angioplasty. Total occlusion with a large amount of myocardium in jeopardy is the postulated prerequisite. In this study, the authors used perfusion balloons instead of standard balloons, so coronary perfusion was maintained and ischemia was minimized. Fourteen patients with standard balloon technique and 11 patients with perfusion balloon technique were studied. The ST segment was less elevated during perfusion angioplasty (0.15 +/- 0.05 mV vs 1.04 +/- 0.19 mV, p<0.001). There were six (43%) patients with ST-T alternans with standard balloon technique compared with none in the perfusion balloon group (p<0.001). In this study, the authors found that there was less ischemia, less ST segment elevation, and lack of ST-T alternans on the intracoronary electrocardiogram during perfusion balloon angioplasty. These findings support the postulate that a large amount of ischemic myocardium is a prerequisite for ST-T alternans.
Pulsus alternans is usually found in patients with reduced systolic ventricular function. We describe a patient with recurrent pulmonary edema, hypertension, bilateral renal artery stenosis, but with normal systolic function. Pulsus alternans was demonstrated in both pulmonary artery, right ventricle, and left ventricle pressures. After successful renal artery revascularization, the pulsus alternans disappeared. This case illustrates that pulsus alternans can be present with diastolic dysfunction of the left ventricle in the absence of systolic dysfunction.
Patient: Female, 46-year-old Final Diagnosis: Coronary artery dissection and stent dislodgement Symptoms: Chest pain Medication: — Clinical Procedure: PCI Specialty: Cardiology Objective: Rare disease Background: Coronary stent dislodgement is rare but carries serious complications like thrombosis, myocardial infarction, disruption of the systemic circulation, and coronary dissection, which can lead to sudden death. Thus, rapid evaluation and intervention are needed to restore blood flow to vital organs. Case Report: A 46-year-old woman with no relevant past medical history except for smoking, presented to the Emergency Department (ED) with left-sided chest pain. The physical exam was unremarkable. EKG showed ST segment elevation, and troponin was 4.03. She underwent cardiac catheterization, which showed 100% occlusion of the left anterior descending coronary artery (LAD). A drug-eluting stent (DES) was placed. Later, she had chest pain similar to the initial episode. EKG showed 1-mm elevation at ST segment in leads V1 and V2 and T wave inversion in leads V2, V3, V4, and V5. She underwent a repeat heart catheterization, which revealed a dissection in the middle LAD distal to the initial stent placement. She was treated with another stent overlapping the proximal stent. While attempting to cross the proximal stent, the stent came off the balloon, slipped from the wire, and went down into the descending aorta. Conclusions: Coronary artery stent dislodgement is a rare event that can lead to significant complications during PCI. Patient restlessness and small-sized, severely angulated, and previously stented coronary arteries are associated risk factors. The main treatment option is stent retrieval, either surgically or using other available techniques. If retrieval of the stent is impossible, crushing it against the blood vessel wall could be considered.
Cardiac troponin I (cTnI), a sensitive and specific marker for myocardial injury, has been utilized for the diagnosis of an acute myocardial infarction. However, a variety of clinical scenarios without evidence of acute coronary syndrome (ACS), such as pulmonary embolism, sepsis, renal failure or stress-induced cardiomyopathy may also cause the elevation of cTnI. We described a 55-year-old Hispanic male with abnormal elevations of cTnI without objective evidence of myocardial infarction damage. We hypothesized that his long-term chronic alcoholic intoxication is causing the myocardial injury, responsive for cTnI elevation. We proposed that alcohol-induced early myocardial damage, independent of alcoholic cardiomyopathy, might be related to alcohol-induced cTnI elevation in this patient. This is the first report suggesting that the abnormal elevations of cTnI can be seen in patients with chronic alcoholism without objective evidence of myocardial infarction.
Acute hyperkalemia can be challenging to recognize clinically since its presentation may be vague. Hyperkalemia can be catastrophic in its outcome, leading to sudden death from cardiac arrhythmias if not recognized and treated emergently. This fact emphasizes the critical need to have a vigilant eye for these cases, provide emergent care, and have timely intervention in order to save patients at risk. We are presenting three cases with hyperkalemia with different outcomes.
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