Ali Farooq

Use of MitraClip for Postmyocardial Infarction Mitral Regurgitation Secondary to Papillary Muscle Dysfunction

Papillary muscle rupture after acute myocardial infarction (AMI) is a dreadful complication and it is associated with five percent of deaths following AMI. Surgery is the recommended treatment of choice; however, it is usually deferred due to the high risk of mortality. MitraClip implantation using a transcatheter approach is an alternative option for patients with severe mitral regurgitation (MR) following AMI or those with high operative risk. We report a case of a 68-year-old male patient who developed severe MR secondary to AMI and underwent successful mitral valve repair using the MitraClip device.

A Case of Recurrent Thrombotic Microangiopathy Caused by Hypertensive Urgency

A 26-year-old man presented to the emergency room with abdominal pain, nausea, and vomiting for four days. His medical history was significant for hypertension and end-stage renal disease managed with hemodialysis. He had been noncompliant with the antihypertensive regimen which included nifedipine, hydralazine, and spironolactone. At presentation, his blood pressure was 231/123 mmHg. Laboratory workup showed white blood count 17.3 × 109/L (normal range: 4.5 to 11.0 × 109/L), hemoglobin 7.8 gm/dL (normal range: 13.5 to 17.5 g/dL), platelet count 46 × 109/L (normal range: 150 to 400 × 109/L), reticulocyte count 7.8%, total bilirubin 1 mg/dL (normal range: 0.1 to 1.2 mg/dL), lactate dehydrogenase 1,235 U/L (normal range: 140 to 280 U/L), haptoglobin < 10 mg/dL, and a direct Coombs test was negative. Numerous schistocytes were identified on the peripheral blood smear. The patient was diagnosed with thrombotic microangiopathy secondary to severe hypertension and was started on intravenous nicardipine. With appropriate blood pressure control, hematological parameters improved with normalization of the platelet count within 10 days. Notably, the patient had one similar episode of hypertension-induced thrombotic microangiopathy within a period of the last three months and ADAMTS-13 (a disintegrin and metalloprotease with thrombospondin type 1 motif 13) activity was normal on his previous admission.

Mitotane-induced dyspnoea: an unusual side effect

Mitotane is a cytostatic antineoplastic agent that is used in the treatment of adrenocortical carcinoma and Cushing’s syndrome. The commonly reported side effects associated with mitotane are anorexia, nausea, vomiting, diarrhoea, decreased memory, rash, gynaecomastia, arthralgias and leucopenia. We present a case of a 68-year-old female who developed gradual dyspnoea concurrent with the use of mitotane for the treatment of adrenocortical carcinoma. To the best of our knowledge and literate review, this is the first reported case of dyspnoea associated with the use of this medication. The purpose of this case report is to raise awareness about this uncommon adverse effect of mitotane that may have gone unrecognised on postmarketing surveillance because of under-reporting, lack of case follow-up or other comorbidities masking shortness of breath.

Gastrointestinal Side Effects of Antiarrhythmic Medications: A Review of Current Literature

Antiarrhythmic drugs are commonly prescribed cardiac drugs. Due to their receptor mimicry with several of the gastrointestinal tract receptors, they can frequently lead to gastrointestinal side effects. These side effects are the most common reasons for discontinuation of these drugs by the patients. Knowledge of these side effects is important for clinicians that manage antiarrhythmic drugs. This review focuses on the gastrointestinal side effects of these drugs and provides a detailed up-to-date literature review of the side effects of these drugs. The review provides case reports reported in the literature as well as possible mechanisms that lead to gastrointestinal side effects.

Fibromuscular Dysplasia with Spontaneous Coronary Artery Disease Presenting as Acute Myocardial Infarction

A 40-year-old female presented to a rural hospital with crushing substernal chest pain. An initial electrocardiogram showed ST elevation in lead II and aVF with elevated troponin I. She was immediately transferred to a tertiary care hospital. An emergent coronary angiogram did not show any significant coronary artery disease. On the second day, the patient experienced recurrence of severe chest pain with ST elevations in leads I, aVL, V5-V6, ST depressions in V1-V3, T-wave inversion over V2-V5. The troponin I level increased to > 40 ng/ml (normal 0.0 to 0.04 ng/ml). An emergent angiogram was performed revealing local dissection of the mid to distal left main coronary artery and a totally occluded diagonal artery. It was deemed unsafe to perform percutaneous coronary intervention because it was a non-flow limiting left main coronary artery dissection and was difficult to cannulate with the guide catheter. Subsequently, an elective angiogram was performed after a 48-hour interval to evaluate the progression of dissection and to make a definitive decision for revascularization versus medical management. On the third angiogram, stenosis seen in the diagonal branch on the previous angiogram progressed to dissection, and local dissection of the left main coronary artery seen on the previous angiogram spontaneously resolved. The patient was symptom-free and hemodynamically stable. It was decided to manage the patient conservatively due to the spontaneous resolution of occlusion in the diagonal artery and dissection of the left main coronary artery. The patient was started on conservative medical treatment. A magnetic resonance angiography of the right internal carotid artery revealed a “string of beads” appearance, which confirmed the diagnosis of fibromuscular dysplasia. She was followed closely in the clinic and has remained asymptomatic for the past one year.

Acute Myocardial Infarction in Young Systemic Lupus Erythematosus Patient with Normal Coronary Arteries

A 34-year-old female with a past medical history of systemic lupus erythematosus (SLE) and a deep venous thrombosis experienced substernal chest pain for 24 hours. Her physical exam was remarkable for brown macular rash over the face. Her initial electrocardiogram showed ST depression in lead V3–V6 along with an elevated troponin I level of 1.23 ng/dl (normal 0.0–0.4) that increased to 2.33 ng/dl in a four-hour duration. Cardiac catheterization revealed mild 10–20% focal plaque in the mid left anterior descending artery and otherwise normal coronary arteries. Laboratory data revealed an erythrocyte sedimentation rate of 98 mm/hour (normal 1–20), C-reactive protein of 25 mg/L (normal 0.0–2.9), and positive antinuclear antibody. In the absence of a significant coronary atherosclerosis along with elevated inflammatory markers, inflammation of coronary microcirculation was considered as an underlying pathophysiology of myocardial infarction. The patient was started on immunosuppression therapy with hydroxychloroquine and prednisone. Her chest pain improved and she was discharged in a stable condition. The patient remained stable and symptom-free over a follow-up period of nine months.