# Unveiling Mixed Apical Hypertrophic Cardiomyopathy: A Case Study on Hypovolemia-Induced Syncope

## TL;DR

This case study describes an elderly woman with a rare heart condition that caused fainting due to dehydration, highlighting the importance of early diagnosis and treatment.

## Contribution

The paper presents a rare case linking hypovolemia-induced syncope with mixed apical hypertrophic cardiomyopathy.

## Key findings

- The patient's syncope was linked to hypovolemia and mixed apical hypertrophic cardiomyopathy.
- Echocardiography confirmed LV apical hypertrophy and LVOT obstruction.
- Treatment with fluids and carvedilol resolved symptoms and highlighted the need for early diagnosis.

## Abstract

Mixed apical hypertrophic cardiomyopathy (MAHCM) is a rare variant of hypertrophic cardiomyopathy characterized by hypertrophy of the left ventricular (LV) apex with septal involvement, increasing the risk of left ventricular outflow tract (LVOT) obstruction, mid-ventricular obstruction, and adverse cardiovascular events such as syncope and sudden cardiac death. We describe an 84-year-old female with a history of hypertension and hyperlipidemia who presented with a syncopal episode preceded by dizziness, blurred vision, and diaphoresis, with a history of poor oral intake and weight loss. She was hemodynamically stable but exhibited orthostatic changes, and laboratory findings revealed acute kidney injury (AKI) suggesting hypovolemia. Electrocardiogram (ECG) showed normal sinus rhythm with left ventricular hypertrophy and repolarization abnormalities, while transthoracic echocardiography (TTE) revealed a hyperdynamic left ventricular ejection fraction (LVEF) of 75%, LV apical hypertrophy with septal involvement, mild systolic anterior motion of the mitral valve leaflet with trace mitral regurgitation, and diastolic dysfunction. The measured LVOT diameter, E/A ratio, E/E' ratio, and septal E' velocity per TTE indicated LVOT obstruction and diastolic dysfunction. The patient was treated with intravenous fluids for hypovolemia and initiated on carvedilol, leading to symptom resolution. Her clinical presentation, ECG findings, and echocardiographic parameters were suggestive of MAHCM, though differentiation from hypertensive heart disease remained a consideration. This case highlights the role of dehydration-induced hypovolemia in precipitating syncope in patients with MAHCM and underscores the importance of recognizing MAHCM in patients presenting with unexplained syncope. Early identification and management are critical in preventing complications such as arrhythmias and sudden cardiac death. Given the demographic variability and under-recognized nature of MAHCM, clinicians should maintain a high index of suspicion in elderly patients with hypertension who exhibit syncope, particularly in the setting of hypovolemia.