🫀⚠️ We’ve been selecting patients for revascularization… wrong.
👉 ischemia = treat... not really?
For years the rule was simple:
👉 find ischaemia
👉 fix the artery
But what if ischaemia is NOT the key?
This editorial on CTO-PCI says something uncomfortable:
👉 Ischaemia does NOT predict outcomes.
Even when:
👉 ≥10% ischaemic burden
👉 PET or SPECT proven
There was:
❌ no reduction in death
❌ no reduction in hard events
So what actually improves?
👉 Symptoms.
👉 Quality of life.
That’s it.
Let that sink in.
We are:
👉 opening complex CTOs
👉 taking procedural risks
👉 chasing ischaemia
But:
⚠️ Ischaemia is NOT driving prognosis.
The real paradigm shift
From: ❌ Ischaemia-driven cardiology
To: 👉 Patient-driven cardiology
The new selection logic:
👉 refractory angina
👉 functional limitation
👉 patient suffering
FIRST.
Imaging?
Still crucial—but:
👉 as a SUPPORT tool, not the decision-maker
Even the paper states it clearly:
👉 Ischaemia alone is an insufficient arbiter for revascularization
And there’s a deeper problem
We love measurable things:
👉 % ischaemia
👉 flow reserve
👉 perfusion maps
But we ignore:
👉 symptoms
👉 daily function
👉 real patient experience
My take
This is the same cognitive error we see everywhere:
👉 We treat numbers
instead of
👉 treating patients
Final thought
If your indication for CTO-PCI is:
👉 “there is ischaemia”
You’re already outdated.
The future is brutally simple:
👉 No symptoms → think twice
👉 Symptoms → act
⚡ Because in modern cardiology:
The most important endpoint is not the image.
It’s the patient.
#Cardiology #CTO #PCI #Ischaemia #Imaging #PrecisionMedicine #CardiacCT #CardiacPET
🫀🏃♂️ Exercise Physiology: Why Fitness Is a Vital Sign
Cardiorespiratory fitness (CRF) isn’t just about performance — it’s one of the strongest predictors of cardiovascular and all-cause mortality. In fact, the American Heart Association recommends treating CRF as a clinical vital sign.
At the center of CRF is VO₂ max — the gold standard measure of maximal oxygen uptake. It reflects the integrated function of:
❤️ Heart (cardiac output)
🫁 Lungs (ventilation & gas exchange)
🩸 Blood (oxygen delivery)
💪 Muscle (mitochondrial extraction & utilization)
Using the Fick equation, oxygen consumption = cardiac output × arteriovenous O₂ difference. In simple terms: how much blood the heart pumps × how much oxygen muscles extract.
📉 Without training, VO₂ max declines ~1% per year with aging — but this decline is attenuated by sustained physical activity.
🔥 Fuel dynamics matter:
At low intensity → fat predominates
At higher intensity → carbohydrates take over
The “crossover” reflects neurohormonal and metabolic shifts.
🧠 Thresholds define performance:
• Ventilatory threshold = sustainable steady-state intensity
• Lactate threshold ≠ “fatigue toxin” — lactate is a metabolic shuttle, not waste
• VE/VCO₂ slope = powerful prognostic marker in heart failure
💓 During exercise, cardiac output can increase ≥5-fold. Stroke volume adaptation — not heart rate — is the primary training-driven cardiac improvement.
🫁 In healthy individuals, lungs rarely limit maximal exercise — it’s usually the heart and peripheral extraction.
🔎 Bottom line:
Exercise is not a single-organ phenomenon. It is a fully integrated systems test of human physiology — and one of the most powerful tools in prevention medicine.
Fitness is not optional biology. It’s measurable resilience.
Patients love our virtual cardiac rehab program, which provides guided exercises to people who have undergone major heart surgery. The best part: It can be done right at home. ❤️💻🏡 Learn more: https://t.co/7nSrp7ZXNk