Pacemaker-Mediated Tachycardia: A Case Report.

Pacemakers respond to the physical activity of patients by increasing the heart rate to compensate for the increased demand. They sense the physical activity of the patient with the help of different types of sensors that work with different mechanisms. In this case, we are presenting a 74-year-old male who was experiencing intermittent chest pain and palpitations. Following interrogation, he was found to have atrial paced tachycardias due to a tracking of the atrial tachycardia.

Delayed Onset Atrioventricular Block After Surgical Aortic Valve Replacement: A Rare Entity.

Surgical aortic valve replacement (SAVR) is the mainstay treatment for aortic valve diseases in patients with low surgical risk. Trans aortic valve replacement (TAVR) has also grown over the past few years, although limited durability data is available. Atrioventricular conduction abnormalities (AVCA) are known complications in the immediate period post-TAVR and SAVR. There are no case reports regarding the development of the delayed onset AVCA years after SAVR. In this case report, we present a male patient who developed a complete heart block six years after SAVR, following which he got the permanent pacemaker implantation (PPMI).

Tacrolimus-Induced Thrombotic Microangiopathy After Orthotopic Heart Transplant: A Case Report.

Tacrolimus (FK 506) is a calcineurin inhibitor and is commonly used as an immunosuppressant after a solid organ transplant. One of the serious adverse effects of tacrolimus is thrombotic microangiopathy (TMA) which has a high mortality rate. TMA leads to vascular thrombosis, eventually leading to ischemia of end organs. It is diagnosed clinically and based on the laboratory parameters. Early detection of TMA and prompt treatment can change the course. Drug-induced TMA has a poor prognosis as compared to idiopathic TMA. We present here the case of a 47-year-old male who developed tacrolimus-induced TMA after an orthotopic heart transplant and he was treated with the currently available treatment. He ultimately died after 40 days of hospitalization.

Arrhythmogenic Right Ventricular Dysplasia (ARVD) With Protein Plakophilin-2 Mutation.

Arrhythmogenic right ventricular dysplasia (ARVD) is a heart muscle disease that predominantly affects the right ventricle; however, biventricular involvement is increasingly being recognized. Fibrofatty tissue replacement is a central feature of ARVD. The majority of the identified genes, including protein plakophilin-2 (PKP-2), involved in cell-to-cell adhesion, can be seen in most genetic cases. Clinically, affected individuals present with palpitations, syncope, or sudden death due to ventricular arrhythmias, such as ventricular tachycardia (VT) or fibrillation, with symptomatic heart failure usually only in later stages. In this study, we present a male patient with ARVD who underwent a genetic test that revealed ARVD with PKP-2 mutation after multiple admissions for heart failure and arrhythmias. He ultimately underwent orthotopic heart transplantation (OHT). Early detection is important for further management, risk stratification, and reduced hospitalization in patients with ARVD.

Catastrophic Events of Cardiac Sarcoidosis: A Case Report.

Cardiac sarcoidosis (CS) can be silent in most patients with extrapulmonary sarcoidosis. Atrioventricular (AV) block is the most common clinical presentation, but it can also present as fatal ventricular arrhythmias and sudden cardiac death. Endomyocardial biopsy is the gold standard; however, it is not sensitive since CS can involve the myocardium in a patchy distribution. Our case depicts a female who presented with syncope; however, her hospital course was complicated by multiple cardiac arrests. Her initial laboratory tests, including an autoimmune workup, were unremarkable. Cardiac magnetic resonance and fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging revealed intramyocardial delayed enhancement of the basal anteroseptal (non-ischemic distribution) and patchy foci of increased uptake in the anteroseptal and inferior myocardial region, respectively. The patient was started on intravenous methylprednisolone, and her condition slowly improved. Post-discharge, the patient followed in the outpatient clinic with a repeat FDG-PET scan revealing resolution of myocardial FDG uptake. She also underwent bronchoscopy with lymph node biopsy showing granulomas and endobronchial biopsy confirming pulmonary sarcoidosis.

A comprehensive review of obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a complex disorder characterized by collapse of the upper airway during sleep. Downstream effects involve the cardiovascular, pulmonary, and neurocognitive systems. OSA is more prevalent in men than women. Clinical symptoms suggest the diagnosis of OSA but none is pathognomonic of the condition. With rising awareness of OSA and the increasing prevalence of obesity, OSA is increasingly recognized as a major contributor to cardiovascular morbidity including systemic and pulmonary arterial hypertension, heart failure, acute coronary syndromes, atrial fibrillation, and other arrhythmias. Pulmonary manifestations include the development of chronic thromboembolic disease, which can then lead to chronic thromboembolic pulmonary hypertension (CTEPH). Neurocognitive morbidities include stroke and neurobehavioral disorders. Screening for OSA includes the use of symptom questionnaires and the diagnosis is confirmed by polysomnography. Management primarily includes the use of continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) devices during sleep. Alternate options such as mandibular devices and surgical procedures are considered for certain patient populations.

A 66-Year-Old Female with Apical Hypertrophic Cardiomyopathy Presenting with Hypertensive Crises and Type 2 Myocardial Infarction and a Normal Coronary Angiogram.

A 66-year-old female presented to the emergency room with an episode of chest pain that lasted for a few minutes before resolving spontaneously. Electrocardiogram showed a left bundle branch block, left ventricular hypertrophy, and T wave inversions in the lateral leads. Initial cardiac troponin level was 0.15 ng/ml, with levels of 4 ng/ml and 9 ng/ml obtained 6 and 12 hours later, respectively. The peak blood pressure recorded was 195/43 mmHg. Echocardiogram with DEFINITY showed a small left ventricular cavity with apical hypertrophy, and coronary angiogram showed no stenotic or occluding lesions in the coronary arteries. The patient was admitted for a type 2 myocardial infarction with hypertensive crises. She was diagnosed with having apical hypertrophic cardiomyopathy, which is a variant of hypertrophic cardiomyopathy (HCM) in which the hypertrophy predominantly involves the apex of the left ventricle resulting in midventricular obstruction, as opposed to the left ventricular outflow tract obstruction seen in HCM. Patients with apical HCM may present with angina, heart failure, myocardial infarction, syncope, or arrhythmias and are typically managed with medications like verapamil and beta-blockers for those who have symptoms and antiarrhythmic agents like amiodarone and procainamide for treatment of atrial fibrillation and ventricular arrhythmias. An implantable cardioverter defibrillator (ICD) is recommended for high-risk HCM patients with a history of previous cardiac arrest or sustained episodes of ventricular tachycardia, syncope, and a family history of sudden death.

Anomalous Aortic Origin of Coronary Arteries from the Opposite Sinus: A Case Report.

Anomalous aortic origin of coronary arteries from the opposite sinus (AAOCA) is a rare finding which, when discovered, raises questions regarding its approach and management. Modern imaging techniques can help us to identify certain anatomical features of the anomalous coronary arteries to further classify them as benign or malignant anomalies. We present a case of a 64-year-old male who had an incidental finding of AAOCA with the left anterior descending artery arising from the right coronary cusp from an ostium anterior to the one that gave rise to both the left circumflex artery and right coronary artery (RCA). The patient was managed with a percutaneous coronary intervention for an obstructive disease of the RCA and was discharged with regular follow-ups.

A Case of Hyperacute Severe Thrombocytopenia Occurring Less than 24 Hours after Intravenous Tirofiban Infusion.

Thrombocytopenia is defined as a condition where the platelet count is below the lower limit of normal (<150 G/L), and it is categorized as mild (100-149 G/L), moderate (50-99 G/L), and severe (<50 G/L). We present here a 79-year-old man who developed severe thrombocytopenia with a platelet count of 6 G/L, less than 24 hours after intravenous tirofiban infusion that was given to the patient during a percutaneous transluminal coronary angioplasty procedure with placement of 3 drug-eluting stents. The patient's baseline platelet count was 233 G/L before the procedure. Based on the timeline of events during hospitalization and laboratory evidence, it was highly likely that the patient's thrombocytopenia was the result of tirofiban-induced immune thrombocytopenia, a type of drug-induced immune thrombocytopenia (DITP) which occurs due to drug-dependent antibody-mediated platelet destruction. Anticoagulant-mediated artefactual pseudothrombocytopenia was ruled out as no platelet clumping was seen on the peripheral blood smears. The treatment of DITP includes discontinuation of the causative drug; monitoring of platelet count recovery; or treatment of severe thrombocytopenia with glucocorticoids, IVIG, or platelet transfusions depending on the clinical presentation. The most likely causative agent of this patient's thrombocytopenia-tirofiban-was discontinued, and the patient did not develop any signs of bleeding during the remainder of his hospital stay. His platelet count gradually improved to 24 G/L, and he was discharged on the sixth hospital day.

Acute Pericarditis Occurring Three Days after Intravesical Instillation of Mitomycin C after Transurethral Bladder Tumor Resection in a 64-Year-Old Woman.

We present a 64-year-old woman who developed symptoms of acute pericarditis three days after undergoing intravesical instillation of mitomycin C following transurethral bladder tumor resection. Mitomycin C is a chemotherapeutic agent which acts by alkylation of DNA and is known to be cardiotoxic when systemically administered. Despite classic pericarditis symptoms, the patient underwent an urgent coronary angiogram due to elevated cardiac troponin I level, EKG changes, and wall motion abnormalities on her echocardiogram. During her angiogram, it was found that she had multiple stenotic coronary artery lesions, with no acute total coronary occlusions, and percutaneous coronary intervention (PCI) was done with placement of a single drug-eluting stent for a 95% stenotic lesion in the left anterior descending artery. The patient was discharged after an uneventful hospitalization on dual antiplatelet therapy with aspirin and prasugrel, and colchicine for pericarditis. It is likely that the patient's presentation was the result of a perimyocardial inflammatory process secondary to intravesically administered mitomycin C, rather than an acute coronary syndrome. While the pathophysiological basis of cardiotoxicity of systemically administered mitomycin C is well documented, more studies are needed to determine whether intravesical MMC may cause cardiotoxicity.