As coronavirus disease 2019 vaccines are being increasingly administered worldwide, subsequent side effects, such as myocarditis, pericarditis, and myopericarditis, are becoming increasingly more common. Our case describes a 64-year-old male who developed chest pain and shortness of breath one week after receiving the Moderna (Cambridge, Massachusetts) COVID-19 mRNA vaccine. He was found to have a large, left-sided pleural effusion and a small pericardial effusion. The patient underwent thoracentesis and video-assisted thoracoscopic procedure with chest tube placement, which drained bloody pleural and pericardial fluid. He was treated with a course of colchicine. Subsequent imaging revealed the resolution of pericardial and pleural effusions, along with the resolution of symptoms.
Pulmonary arterial hypertension (PAH), characterized as a resting mean pulmonary artery pressure greater than 25 mmHg, is due to the narrowing of the pulmonary arteries, which can be idiopathic, inherited, or drug-related. Alkylating agents, including cyclophosphamide, are a risk factor for developing the pulmonary veno-occlusive disease. Drug-induced PAH is extremely rare. A 59-year-old female with newly diagnosed invasive ductal carcinoma of the right breast and high-grade ductal carcinoma in situ of the left breast was initiated treatment with doxorubicin and cyclophosphamide. About one week after receiving the first cycle, the patient developed worsening lower extremity edema and shortness of breath. She was then hospitalized, and a transthoracic echocardiogram and coronary angiogram revealed PAH. The team then changed the breast cancer treatment regimen to Taxol and carboplatin, and PAH was resolved in a follow-up echocardiogram after five months. This report has described the first case of PAH directly related to cyclophosphamide and doxorubicin. It is imperative to promptly recognize this rare but important sideeffect as early diagnosis and response can potentially reverse the disease progression.
Currently, ivabradine is not approved for the treatment of sinus tachycardia secondary to hyperthyroidism. We aimed to increase the recognition of ivabradine as an effective alternative to, or combination with, beta-blockers in controlling sinus tachycardia secondary to hyperthyroidism. Elevated thyroid hormone levels enhance cardiac performance through a positive chronotropic effect, resulting in an increased heart rate (HR), an effect brought on by increasing the
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funny current at sinoatrial node (SAN). Ivabradine is a novel, dose-dependent selective inhibitor of
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channels. By decreasing SAN pacemaker activity, ivabradine allows for selective reduction of HR with a resultant increase in ventricular filling time. This mechanism sets ivabradine apart from the typical rate-reducing medications, namely beta-blockers and calcium channel blockers, which simultaneously decrease HR and myocardial contractility. We describe a case of hyperthyroidism-induced sinus tachycardia, resistant to maximal doses of beta-blocker, which was successfully managed by ivabradine. After excluding other causes of tachycardia, such as anemia, hypovolemic states, structural heart disease, drug abuse, and infection, ivabradine was given off-label for symptomatic relief of hyperthyroidism-induced sinus tachycardia. Within 24 h, HR steadily decreased to the low 80s. Our patient had a unique presentation in which he presented with hyperthyroidism-induced sinus tachycardia with no relief after administration of maximal dose of beta-blocker. Ivabradine was then given, with resolution of sinus tachycardia within 24 h.
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