Lyme carditis represents a rare cardiac complication of Borrelia burgdorferi infection, often causing conduction disturbances but rarely causing malignant arrhythmias. Inflammatory acute coronary syndrome, driven by immune-mediated plaque erosion rather than rupture, represents a nontraditional ischemic mechanism. This case highlights their overlap. The case of a previously healthy man with Lyme disease who experienced cardiac arrest because of ventricular tachycardia is reported. Imaging showed myocardial inflammation together with coronary plaque erosion instead of plaque rupture. The patient underwent advanced diagnostic testing and received multidisciplinary medical care, which led to complete cardiac recovery and implantable cardioverter-defibrillator placement.

This case study explores the journey of an 80-year-old male patient with a history of hypertension, diabetes, coronary artery disease after coronary artery bypass grafting, atrial fibrillation, and heart failure. Nine months before he presented to the emergency department, he had undergone mitral valve clipping for severe mitral valve regurgitation. Despite initial improvement, the patient experienced return of symptoms, including dyspnea at rest and lower limb edema. The results of this case-discovery of the need for mitral valve replacement-provides insights into the management of complications from mitral valve clipping and emphasizes that management requires a nuanced, meticulous approach.

Key pathobiological components of ischemic heart disease have been identified as follows: (1) In 1970 to 1973, myocardial infarct size was found to be the primary determinant of prognosis after acute myocardial infarction (AMI); (2) in 1973 to 1989, vulnerable coronary artery plaques were found to predispose individuals to coronary plaque disruption and thrombosis, causing major AMI; (3) in 1972, timely coronary reperfusion was demonstrated to limit the size of evolving AMI but with risk of reperfusion injury; and (4) in 1986, myocardial conditioning was found to be a clinically significant modulator capable of delaying AMI progression. Promising cardioprotective strategies combining timely reperfusion with conditioning in experimental animal and proof-of-concept human studies have not been shown to optimize cardioprotection, and this area of research has stalled. Nevertheless, opportunities for further progress against ischemic heart disease have come from new perspectives and approaches, including (1) recognition that functionally significant ischemic heart disease can result from microvascular dysfunction or epicardial coronary atherosclerosis; (2) rapid diagnosis of AMI subtypes through application of the Universal Definition of Myocardial Infarction based on high-sensitivity cardiac troponin measurements; (3) the Canadian Cardiovascular Society classification of AMI based on stages of tissue injury severity, as detected by advanced imaging; (4) implementation of the occlusion vs nonocclusion MI paradigm to prompt aggressive management of all ST-segment elevation MI and the one-third of non-ST-segment elevation MI with total occlusion; and (5) implementation of the Early Heart Attack Care program, which emphasizes prodromal symptom recognition to prevent AMI progression.

A 63-year-old man with a history of hypertension, prediabetes, and sleep apnea presented with pedal edema, weight loss, and flushing. Laboratory work revealed elevated B-type natriuretic peptide and normocytic anemia. Echocardiography showed right ventricular enlargement, severe tricuspid valve regurgitation, and thickened tricuspid valve leaflets, raising suspicion for carcinoid heart disease. Further testing confirmed a neuroendocrine tumor with liver metastasis. Despite somatostatin therapy, the patient's symptoms were refractory to diuretics. Surgical intervention with tricuspid and pulmonary valve replacement was undertaken. Postoperatively, the patient demonstrated substantial improvement in functional tolerance and quality of life. This case highlights the importance of surgical intervention in advanced carcinoid heart disease.

This report highlights a case of early structural valve deterioration with a cusp tear in a second-generation Abbott Trifecta Glide Technology bioprosthetic heart valve. A 70-year-old man had undergone aortic valve replacement with a Trifecta Glide Technology valve 30 months earlier for severe bicuspid aortic valve stenosis. He suddenly developed acute heart failure with dyspnea resulting from severe aortic valve regurgitation, with a cusp tear in the Trifecta Glide Technology valve, as demonstrated by transthoracic echocardiography. The patient was successfully treated with urgent repeat aortic valve replacement.

The Micra device is a leadless pacemaker implanted in the right ventricle via a femoral vein transcatheter approach. There are several indications for and advantages to using a leadless pacemaker, and the device's role in the field of cardiology will probably continue to increase. This article presents the case of a rare complication probably due to inadvertent placement of the device in the left ventricle across an undiagnosed patent foramen ovale.

Rhabdomyosarcoma represents almost 20% of all primary malignant neoplasms of the heart. In the majority of cases, the tumor arises from the ventricular wall, although these tumors can also arise from the atrial walls and mimic atrioventricular valve stenosis. This report presents a case of a patient diagnosed with an atrial mass that was detected by transthoracic echocardiography and confirmed by histopathology. The mass was successfully resected during an uneventful surgical intervention, but the patient died 6 months after the procedure.

Platypnea-orthodeoxia syndrome is a rare condition characterized by positional dyspnea and hypoxemia, with symptoms presenting in the upright position and improving when recumbent. Hypoxemia in platypnea-orthodeoxia syndrome is defined as a drop in Pao2 of more than 4 mm Hg or oxygen saturation greater than 5% when moving from a supine to an upright position. Etiologic mechanisms include intracardiac or pulmonary shunts and ventilation perfusion ratio mismatch. Platypnea-orthodeoxia syndrome has been described as part of COVID-19 pneumonia sequelae, with differing physiologic mechanisms from cardiac pathologies. This report presents the case of a patient with platypnea-orthodeoxia syndrome of multifactorial etiology: intracardiac shunting secondary to a patent foramen ovale and ventilation perfusion ratio mismatch as a sequela of COVID-19 pneumonia.