Delayed Presentation of a Post-infarction Ventricular Septal Rupture.

Ventricular septal rupture, a formidable complication of acute myocardial infarction (AMI), is linked to significant morbidity and mortality. The clinical manifestation typically involves pronounced hemodynamic compromise necessitating prompt surgical intervention. This report outlines the case of a 60-year-old male presenting with acute heart failure 3 weeks post a presumed AMI. On evaluation, a substantial ventricular septal defect with left-to-right shunt was observed. The patient, although hemodynamically stable with mild symptoms, underwent surgical closure of the defect and coronary artery bypass graft for multivessel coronary artery disease. This case contributes to the literature on the delayed presentation of post-myocardial infarction (MI) ventricular septal rupture, a scenario deviating from the anticipated severe hemodynamic instability given the timing of the MI and the extent of the septal defect.

New-Onset Heart Failure and Ischemic Stroke in Non-compaction Cardiomyopathy: A Case Report.

Left ventricular non-compaction (LVNC) cardiomyopathy is an embryological disorder of endocardial trabeculation and can cause heart failure, arrhythmias, and thromboembolism. Lifelong anticoagulation is indicated in patients with reduced ejection fraction due to high risks of thromboembolism. Reduced ejection fraction can develop in these patients as a consequence of this cardiomyopathy, thereby increasing the risk of intracardiac thrombus formation. This new-onset reduced ejection fraction may develop rapidly, which may not be amenable to detection by routine screening. We present a case of non-compaction cardiomyopathy (NCC) with a previously normal ejection fraction who had an ischemic stroke and was found to have new-onset reduced ejection fraction.

Persistent Heart Failure Despite Medical Therapy Leading to a Diagnosis of Cardiac Amyloidosis.

Cardiac amyloidosis is restrictive cardiomyopathy, commonly classified as either light-chain amyloidosis (AL) or transthyretin amyloidosis (ATTR), which can be further subdivided into wild-type (systemic senile amyloidosis) and hereditary ATTR amyloidosis. Advanced-stage, silent, and clinically undiagnosed amyloidosis has a poor prognosis, with a survival rate of six months and up to five years. We present a 72-year-old female with a past medical history of heart failure, with preserved ejection fraction, atrial fibrillation, systemic lupus erythematosus (SLE), and stage 3b chronic kidney disease, who presented with persistent shortness of breath, lower extremity pitting edema, jugular venous distension, and dyspnea despite optimal medical therapy. The patient was diagnosed with preserved heart failure in the past and was on guideline-directed medical therapy for over five years with no history of cardiac disease in the family. The patient's previous echocardiogram revealed an ejection fraction of 65%. In order to determine the etiology of the patient's cardiomyopathy, she underwent cardiac magnetic resonance imaging (CMR), monoclonal gammopathy testing, and a Technetium pyrophosphate (99mTc-PYP) scintigraphy, of which the latter two were unrevealing. The CMR revealed increased wall thickness and multiple segments of midmyocardial to subendocardial late gadolinium enhancement, suggestive of infiltrative disease. Due to inconclusive testing, the patient underwent an endomyocardial biopsy and was determined to have wild-type, systemic senile amyloidosis, which held a poor prognosis. The patient was started on tafamidis, a new Food and Drug Administration (FDA)-approved therapy for systemic senile amyloidosis, and was discharged on the new medication, with frequent follow-up visits scheduled. Current treatment guidelines for cardiac amyloidosis include loop diuretics and spironolactone. Medications such as beta-blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers are not clinically effective. There are currently new medications on the horizon, such as tafamidis, which stabilizes the transthyretin tetramer and reduces the formation of amyloid. This case highlighted that patients who have persistent symptoms of heart failure, despite guideline-directed medical therapy, and without a history of genetic cardiac conditions, may also have a diagnosis of cardiac amyloidosis. Cardiac amyloidosis is often misdiagnosed or diagnosed late in the disease course; therefore, there is a need for increasing awareness of early diagnosis and treatment, including new FDA-approved medications for a better chance of survival.