Pathophysiology

Pathophysiology

P-I-7. Obesity–Diabetes, Case 3

肥満・糖尿病 症例3

A 62-year-old female patient visits her GP complaining about chest pain caused by physical activity. She has been more tired in recent months, and when she arrives at her flat on the second floor she has palpitations and complaints about the sensation of “something pushing on her chest”. She has been smoking for 40 years: a couple of cigarettes a day.

  • ECG at rest: left deviation, frequency: 72/min
  • ECG on stress: frequency 138/min, negative T waves in V2-V4
  • Blood pressure at rest: 160/85 Hgmm
  • Body height: 165 cm
  • Body weight: 88 kg
  • Abdominal circumference: 98 cm

Laboratory results (fasting):

  • Glucose: 6.9 mmol/l
  • Na⁺: 142 mmol/l
  • K⁺: 4.5 mmol/l
  • Cl⁻: 106 mmol/l
  • HCO₃⁻: 23 mmol/l
  • BUN: 4 mmol/l
  • Kreatinin: 102 μmol/l
  • ASAT: 22 U/L
  • ALAT: 24 U/L
  • ALP: 41 U/L
  • T. bilirubin: 15 μmol/l
  • D. bilirubin: 3.3 μmol/l
  • Total cholesterol: 6.5 mmol/L
  • Triglicerid: 1.9 mmol/L
  • No glucose or ketone present in the urine.

OGTT result 2 days later:

  • fasting result: 6.4 mmol/l
  • result after 2 hours: 8.5 mmol/l

Key Quotes & What They Tell Us

Quote / Value Interpretation
“chest pain caused by physical activity … something pushing on her chest” + palpitations climbing stairs Exertional (stable) angina — pain reproducibly provoked by increased cardiac demand
“smoking for 40 years” Major modifiable coronary risk factor
Stress ECG: HR 138/min with “negative T waves in V2–V4” Inducible myocardial ischaemia in the anterior leads — supports coronary artery disease
OGTT: fasting 6.4 mmol/L, 2-hour 8.5 mmol/L Impaired fasting glucose + impaired glucose tolerance → prediabetes (not yet overt diabetes)
Weight 88 kg, height 165 cm (BMI ≈ 32.3); abdominal circumference 98 cm Obesity with central (visceral) fat distribution
BP 160/85 mmHg; total cholesterol 6.5 mmol/L Hypertension and dyslipidaemia

Key Points

  • Diagnosis: Stable angina pectoris from coronary artery disease, with prediabetes (impaired fasting glucose and impaired glucose tolerance).
  • Pathophysiology: Atherosclerotic coronary narrowing → oxygen supply–demand mismatch during exertion → reversible ischaemia (ECG changes on stress only).
  • Metabolic syndrome: Central obesity, hypertension, dyslipidaemia, dysglycaemia — plus long-standing smoking.
  • Risk clustering: Multiple factors multiply cardiovascular risk; prediabetes can progress to overt type 2 diabetes.
  • Management focus: Smoking cessation, weight loss, and control of glucose, lipids, and blood pressure.

一問一答

What characterizes the pain of stable angina?

Chest pain/pressure reproducibly provoked by exertion and relieved by rest, reflecting a transient oxygen supply–demand mismatch.

What is the diagnosis in a smoker with exertional chest pain, palpitations on climbing stairs, and stress-induced T-wave changes?

Stable angina pectoris due to coronary artery disease.

What metabolic syndrome features does this patient have?

Central obesity (BMI ~32, waist 98 cm), hypertension (160/85), dyslipidaemia (cholesterol 6.5), and dysglycaemia (prediabetes).

Why do negative T waves in V2–V4 appear only on the stress ECG?

They indicate inducible anterior myocardial ischaemia that appears when cardiac demand rises but is absent at rest.

How is prediabetes defined by this patient's OGTT (fasting 6.4, 2-hour 8.5 mmol/L)?

Impaired fasting glucose plus impaired glucose tolerance — prediabetes, not yet overt diabetes.

What is the underlying pathophysiology of stable angina?

Atherosclerotic coronary narrowing limits flow, so during exertion oxygen demand outstrips supply, causing reversible ischaemia.

Why is 40 years of smoking significant in this case?

It is a major modifiable risk factor that accelerates coronary atherosclerosis.

Why does clustering of cardiovascular risk factors matter?

Multiple factors (smoking, obesity, hypertension, dyslipidaemia, dysglycaemia) multiply rather than simply add to overall cardiovascular risk.

What is the management focus for this patient?

Smoking cessation, weight loss, and control of glucose, lipids, and blood pressure.

Why may prediabetes still warrant aggressive intervention?

It can progress to overt type 2 diabetes and already adds to cardiovascular risk.

Why is the resting ECG relatively normal while ischaemia appears only on stress?

At rest coronary flow meets demand; ischaemic ECG changes are unmasked only when demand increases.

What does an abdominal circumference of 98 cm indicate in this woman?

Central (visceral) obesity, which is strongly linked to insulin resistance and cardiovascular risk.

Why is there no glucose or ketone in this patient's urine despite metabolic syndrome?

Her glucose is only mildly elevated (prediabetic range), below the renal glucose threshold, and she is not in a ketotic state.

Why does the heart rate rise to 138/min during the stress test?

Exercise increases sympathetic drive and cardiac demand, which provokes the ischaemia seen on ECG.

How does obesity contribute to coronary artery disease in this patient?

It promotes insulin resistance, dyslipidaemia, and hypertension, all of which accelerate atherosclerosis.

Why is an OGTT useful when fasting glucose is only borderline?

It can reveal impaired glucose tolerance (a post-load elevation) that fasting glucose alone may miss.

Why is smoking cessation the single most important intervention here?

It is the dominant modifiable factor; stopping markedly reduces further coronary risk.

What is the significance of the sensation of 'something pushing on the chest'?

It describes the pressure-like quality typical of ischaemic angina rather than sharp musculoskeletal pain.

Why is her renal function essentially normal in this case?

Creatinine and BUN are within normal limits, indicating no diabetic or hypertensive nephropathy yet.

What does the combination of stable angina plus prediabetes teach about cardiovascular prevention?

Coronary disease can already be present before overt diabetes, so early multi-risk-factor control is essential.