# Elevated Lipoprotein(a)-Associated Coronary Artery Disease in a 45-Year-Old Male

**Authors:** Fatima Abeer, Aasim A Wani, Ali Ahraz

PMC · DOI: 10.7759/cureus.81684 · 2025-04-04

## TL;DR

A 45-year-old man with high lipoprotein(a) and heart disease showed improvement with intensive medical treatment when surgery was not possible.

## Contribution

This case emphasizes the role of elevated Lp(a) in premature CAD and the effectiveness of medical therapy in managing it.

## Key findings

- The patient had markedly elevated Lp(a) levels and significant coronary artery blockages.
- Intensive medical therapy led to symptomatic improvement and better heart function.
- Revascularization was deferred due to financial constraints, but medical management was effective.

## Abstract

Premature coronary artery disease (CAD) in younger adults often arises from underrecognized risk factors such as elevated lipoprotein(a) (Lp(a)), a genetically determined lipoprotein with atherogenic and prothrombotic properties. We report a 45-year-old male with untreated hypertension, prior ischemic stroke, and significant tobacco use, who presented with exertional angina. Laboratory evaluation showed mildly elevated low-density lipoprotein cholesterol (LDL-C; 142 mg/dL), borderline low high-density lipoprotein cholesterol (HDL-C; 38 mg/dL), and markedly elevated Lp(a) (180 mg/dL). Coronary angiography revealed a chronic total occlusion of the proximal left anterior descending (LAD) artery, 90% stenosis of the left circumflex (LCx) artery, and Rentrop grade 3 collateral flow from a codominant right coronary artery. Due to financial constraints, revascularization was deferred. The patient was managed with high-intensity statins, dual antiplatelet therapy, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and lifestyle modification. Over follow-up, he showed marked symptomatic improvement, enhanced left ventricular ejection fraction, and partial reversal of diastolic dysfunction. This case highlights the importance of Lp(a) screening in premature CAD and demonstrates that intensive medical therapy can stabilize high-risk patients when revascularization is not feasible.

## Linked entities

- **Diseases:** coronary artery disease (MONDO:0005010), ischemic stroke (MONDO:1060198)

## Full-text entities

- **Genes:** LPA (lipoprotein(a)) [NCBI Gene 4018] {aka AK38, APOA, LP}
- **Diseases:** ischemic stroke (MESH:D002544), diastolic dysfunction (MESH:D018487), hypertension (MESH:D006973), CAD (MESH:D003324), exertional angina (MESH:C564288)
- **Chemicals:** antiplatelet (-)
- **Species:** Homo sapiens (human, species) [taxon 9606], Nicotiana tabacum (American tobacco, species) [taxon 4097]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12049667/full.md

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Source: https://tomesphere.com/paper/PMC12049667