Diastolic dysfunction is an echo finding — HFpEF is the clinical syndrome you treat
QCG imaging talk for GPs: how to explain “suck and push” to patients, why isolated grade 1 with a normal left atrium rarely becomes HFpEF, and why treatment is “doing the boring stuff well” — Goldilocks loop diuretics plus SGLT2 inhibitors and comorbidity control.
- Speaker
- Dr Nikki Mai (ASR: Nikki Mai / Dr May / Ni Mai) — director of cardiac imaging; cardiac CT and echo specialist. Frames diastology for the GP when the patient arrives with a report and a “so what?”
- Session host / chair
- QCG conference host (first name not clearly captured in this Otter slice; same weekend as cardiovascular education / cardiology subspecialties panels). Brief Q&A tail references Mona and cardio-oncology talks from the same day.
- Session context
- Otter id
RJR657KbEI92kurGwC7G4KKG-rw· title Diastolic Dysfunction Seminar · ~20.2 min (1210 s) · 2026-02-28. Companion: cardiology-subspecialties · cardiovascular-education-weekend · cardiac-case-panel.
Key messages for GPs
- Diastolic dysfunction on an echo letter is a categorical finding. HFpEF is the clinical heart-failure syndrome. They are related but not interchangeable.
- Most people with diastolic dysfunction do not have HFpEF. Every patient with HFpEF has diastolic dysfunction.
- Isolated grade 1, normal LA volume, no cardiometabolic risk — often aging; progression to HFpEF cited as probably <5% over 10 years unless diabetes, obesity, hypertension, CKD or AF arrive.
- HFpEF needs symptoms/signs of congestion plus objective raised filling pressures (echo / BNP / clinical) with LVEF typically ≥50%.
- Treat congestion with loop diuretics in the Goldilocks zone (euvolemia — not over-diuresis). Decongestion improves symptoms but does not by itself cut mortality — SGLT2 inhibitors do reduce hospitalisation and death with or without diabetes.
- ~50% of heart failure now sits with preserved systolic function; normal LVEF does not rule HF out.
Patient language: suck, push, soggy lungs
Mai opens with the consultation problem: “Mr Smith, you have diastolic dysfunction” → “So what?” His fix is physiology in plain English. The heart is a pump with two actions: it sucks (diastole — drawing blood from the lungs) and it pushes (systole). If sucking is impaired, flow into the left heart is poor, pressure backs into the lungs, the lungs get “soggy”, and the patient gets short of breath.
That story links the echo label to the symptom the patient actually cares about — and separates “is it my weight, my diastolic dysfunction, or something else?” into a shared plan rather than a mysterious report phrase.
Echo finding ≠ HFpEF
In the echo lab, diastology is phases, flow patterns and the exam grades (1 / 2 / 3). Those grades matter to imagers; the patient wants breathlessness fixed. Clinically, diastolic dysfunction sits on a spectrum. Echo parameters set the scene — they do not automatically equal HFpEF.
“Normal chamber sizes, grade 1 diastolic dysfunction, no evidence of raised LV end-diastolic pressure” → usually do not refer for “diastolic dysfunction” alone. There is no clinical heart-failure syndrome to treat.
HFpEF (speaker: “heart failure with preserved systolic function”) is the clinical syndrome: exertional breathlessness, PND, peripheral oedema, LVEF typically ≥50% by volumetric analysis, plus objective raised filling pressures (echo markers, BNP, or clear clinical congestion). About half of heart failure now sits in this preserved-EF bucket; prognosis is still poor if advanced grades go untreated.
Patient myth-busting Mai uses: “EF 55% — why isn’t it 100%?” Explain stroke volume as fraction of end-diastolic volume displaced each beat — hearts are not meant to empty completely. Rough ranges he quotes: ~50% normal; 50–55% low-normal; then graded reduction.
Two clinic profiles
| Profile | Echo / labs | Action from the talk |
|---|---|---|
| 72-year-old, murmur, no exertional limit, no diabetes/CKD | Early / grade 1 DD, normal LA volume, no raised filling pressure | Often aging physiology. Rare progression to HFpEF (~<5%/10 y cited) unless comorbidities appear. |
| 78-year-old, exertional dyspnoea, ankle oedema | EF 60%, moderately enlarged LA, elevated LVEDP markers, BNP high | This is HFpEF — congested, needs treatment, not reassurance that “EF is fine”. |
Comorbidities that sharply raise progression risk: diabetes, obesity, hypertension, kidney disease, AF. Shortness of breath is often misattributed — which is why HFpEF stays under-recognised even among specialists.
Treatment: boring stuff done well
Mai’s punchline: HFpEF care is not wires, plugs or calcified-valve theatre — it is “doing the boring stuff well.”
- Treat congestion first — usually a loop diuretic (frusemide). Aim for euvolemia: JVP, dry weight, ankles. Do not over-diurese — these ventricles depend on filling pressure; over-diuresis → hypotension and feeling worse after a brief “better”.
- Decongestion alone does not improve mortality — it makes people feel better. That is necessary but incomplete.
- SGLT2 inhibitors — reduce HF hospitalisation and death with or without diabetes (speaker emphasis).
- ACE inhibitors / antagonists used as comorbidity tools (especially BP) with variable mortality data in this space as framed in the talk.
- Comorbidity management + exercise training — hypertension, diabetes, obesity, CKD, AF — “things you can’t simply give a pill for.”
Enough diuretic to clear lungs and oedema; not so much that preload-dependent diastole collapses into dizziness and renal hit. Reassess volume every time you titrate.
Why SGLT2 inhibitors help
Two mechanisms Mai highlights:
- Osmotic diuresis + natriuresis — preferential interstitial fluid loss versus loop diuretics’ heavier intravascular hit → less hypotension / neurohormonal activation.
- Myocardial fuel shift — among glucose, free fatty acids and ketones, ketones are the most ATP-efficient per oxygen molecule; strained myocardium with inefficient mitochondria benefits from that pathway. Renal protection is a wanted extra.
Clinic checklist
- Read the whole echo letter: grade, LA size, filling-pressure comment, LVEF — not the word “diastolic” alone.
- Match to symptoms: if congested + raised pressures → treat as HFpEF; if isolated grade 1 → educate, risk-factor watch, avoid over-referral panic.
- Explain EF as volume displacement, not a “percentage of life left.”
- Diuretic: titrate to euvolemia; warn about over-diuresis.
- Offer / continue SGLT2 where indicated for HFpEF phenotype; attack the comorbidity cluster; prescribe exercise as medicine.