# Successful large caloric deficit with high protein modification diet and intensive aerobic and resistance training with progressive overload in adult patient with significant coronary artery disease: a case report

**Authors:** Reynard Laysandro, Elbert Aldrin Harijanto, Nicky Alexandra Sie

PMC · DOI: 10.3389/fcvm.2026.1737431 · Frontiers in Cardiovascular Medicine · 2026-02-04

## TL;DR

A man with severe obesity and heart disease successfully lost 50 kg through a strict diet and intense exercise under medical supervision.

## Contribution

Demonstrates feasibility of extreme lifestyle intervention in high-risk coronary artery disease patients with multidisciplinary oversight.

## Key findings

- Patient lost 50 kg (41% of baseline) with significant improvements in waist, visceral fat, and functional capacity.
- Blood pressure and HDL improved, though LDL and total cholesterol increased during the intervention.
- No arrhythmia or ischemic changes observed despite intensive exercise and caloric restriction.

## Abstract

Lifestyle modification plays a central role in obesity and cardiometabolic disease management; however, its application in patients with obstructive coronary artery disease (CAD) is typically cautious due to safety concerns. Caloric restriction with a high protein diet and high-intensity exercise has not been well studied in this setting.

A 43-year-old man with Class III obesity (BMI 43.8 kg/m²), uncontrolled hypertension and severe proximal LAD stenosis (CAD-RADS 4) presented with shortness of breath for evaluation. He declined percutaneous coronary intervention and chose structured intensive lifestyle therapy. Baseline data: waist 125 cm, BP 185/100 mmHg, visceral fat ∼40%, LDL 1.51 mmol/L, HDL 0.97 mmol/L, HbA1c 5.3%, stress METS 6.3 without ischemia.

Under weekly multidisciplinary supervision (internal medicine, cardiology, nutrition, sports medicine), he followed progressive caloric restriction with a high protein diet and high-intensity aerobic plus resistance exercise over 10 months. Usual cardiovascular medical therapy was continued. Monitoring included vitals, ECG, electrolytes, lipids, and exercise tolerance.

The patient lost 50 kg (41% of baseline) with BMI 25.8 kg/m², waist 85 cm, visceral fat 12%. Functional capacity improved (METS 6.30–11.5), HDL increased (0.97–1.63 mmol/L), HbA1c decreased (5.3%–4.9%), and blood pressure improved (185/100 to 140/85 mmHg). However, LDL and total cholesterol rose (LDL 1.51–3.44 mmol/L; total cholesterol 3.32–5.47 mmol/L). LDL rose consistent with fat mobilization physiology during diet and exercise. No arrhythmia or ischemic ECG changes were observed. The patient remained asymptomatic and entered maintenance training.

Extreme supervised lifestyle intervention may be feasible in carefully selected high-risk CAD patients. Standard moderate programs remain recommended; extreme strategies require intensive medical oversight.

## Linked entities

- **Diseases:** obesity (MONDO:0011122), coronary artery disease (MONDO:0005010)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, PTEN (phosphatase and tensin homolog) [NCBI Gene 5728] {aka 10q23del, BZS, CWS1, DEC, GLM2, MHAM}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}
- **Diseases:** myocardial ischemia (MESH:D017202), cardiovascular disease (MESH:D002318), myocardial infarction (MESH:D009203), dizziness (MESH:D004244), insulin resistance (MESH:D007333), leukocytosis (MESH:D007964), Weight reduction (MESH:D015431), repolarization abnormalities (MESH:D000014), rhabdomyolysis (MESH:D012206), LAD stenosis (MESH:C535887), ischemic ST depression (MESH:D000088323), atherogenesis (MESH:D050197), micronutrient deficiency (MESH:D007153), hypertension (MESH:D006973), Caloric restriction (MESH:D002313), hyperuricemia (MESH:D033461), Excess adiposity (MESH:D018205), depression (MESH:D003866), loss of lean body mass (MESH:D013851), thyroid disease (MESH:D013959), cardiac disease (MESH:D006331), CAD-RADS (MESH:D003324), diabetes (MESH:D003920), lung lesions (MESH:D008171), ischemic (MESH:D002545), endothelial dysfunction (MESH:D014652), Dyspnea (MESH:D004417), renal failure (MESH:D051437), alcohol and drug abuse (MESH:D019966), reduced blood volume (MESH:D001523), ventricular dysfunction (MESH:D018754), angina (MESH:D000787), presyncope (MESH:D013575), cardiometabolic disease (MESH:D024821), fluid overload (MESH:D019190), fibrosis (MESH:D005355), inflammation (MESH:D007249), disease (MESH:D004194), injury (MESH:D014947), electrophysiologic disturbances (MESH:D014832), coronary disease (MESH:D003327), coronary syndrome (MESH:D054058), dyslipidemia (MESH:D050171), ischemia (MESH:D007511), caloric deficit (MESH:D009461), stenosis (MESH:D003251), metabolic dysregulation (MESH:D021081), coronary artery stenosis (MESH:D023921), Reduced body mass (MESH:C536030), Class III obesity (MESH:D009765), Arrhythmias (MESH:D001145), weight regain (MESH:D055191), pleural effusion (MESH:D010996), Chest Pain (MESH:D002637)
- **Chemicals:** amino acid (MESH:D000596), vitamin D3 (MESH:D002762), urea (MESH:D014508), niacin (MESH:D009525), carbohydrate (MESH:D002241), -reported adherenc (-), superoxide (MESH:D013481), clopidogrel (MESH:D000077144), hydrogen peroxide (MESH:D006861), amlodipine (MESH:D017311), T3 (MESH:D014284), ROS (MESH:D017382), rosuvastatin (MESH:D000068718), glucose (MESH:D005947), lipid (MESH:D008055), cortisol (MESH:D006854), urate (MESH:D014527), omega-3 (MESH:D015525), vitamin K2 (MESH:D024482), triglyceride (MESH:D014280), vitamin D (MESH:D014807), Oxygen (MESH:D010100), allopurinol (MESH:D000493), Fiber (MESH:D004043), sugars (MESH:D000073893), fish oil (MESH:D005395), nitric oxide (MESH:D009569), Cholesterol (MESH:D002784), aspirin (MESH:D001241), free fatty acids (MESH:D005230)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** RPE — Homo sapiens (Human), Telomerase immortalized cell line (CVCL_4388)

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## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12913545/full.md

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Source: https://tomesphere.com/paper/PMC12913545