Cardiovascular desease

This website is for informational purposes only and not a substitute for medical advice.

Summary

  • This factor describes whether you have had CVD yourself, and whether close relatives had early CVD. Both signal higher long-term risk.
  • A past CVD event increases the chance of dying from many causes because it raises the risk of future heart and vascular events and often comes with other health problems.
  • Across studies, having prior CVD is linked to higher all-cause mortality versus no CVD, with pooled risk estimates reported around 1.24–4.92 depending on the event type and population.
  • Family history of premature CVD (in a first-degree relative) is linked to higher risk of earlier CVD (about 1.7–2.2× in some studies) and is also associated with higher all-cause mortality, especially when multiple relatives are affected.

Factor description

  • Personal CVD history means you have previously been diagnosed with, or treated for, a heart or blood-vessel condition.
    • Examples often include heart attack (myocardial infarction), stroke or TIA, angina, heart failure, peripheral artery disease, atrial fibrillation, or procedures such as PCI (stent) or CABG (bypass).
  • Family history of CVD means close biological relatives have had CVD, especially at younger ages.
    • Usually this focuses on first-degree relatives (parents, siblings, children).
    • “Premature” CVD is commonly defined as before age 55 in men and before age 65 in women.
  • Measurement is typically self-report (what you know about your own diagnoses and your relatives’ diagnoses), sometimes supported by medical records.

Impact on all-cause mortality

  1. Why personal CVD history affects all-cause mortality

    • A prior CVD event raises the risk of another event (repeat heart attack, stroke, heart failure worsening, sudden cardiac death).
    • CVD is also a marker of whole-body vascular disease and metabolic risk (high blood pressure, high LDL cholesterol, diabetes, smoking history), which can affect many causes of death.
    • Many people with CVD have multiple conditions at the same time (for example kidney disease, diabetes, frailty), which increases overall mortality risk.

  2. What studies typically show for personal CVD history

    • Compared with people without CVD, people with prior CVD have higher all-cause mortality.
    • Reported risk estimates vary widely (roughly 1.24–4.92 in pooled estimates in the text you provided), often depending on:
      • the type of index event (heart attack vs stroke vs heart failure)
      • how long ago it happened
      • age and other diseases
      • treatment quality and risk-factor control

  3. Why family history affects all-cause mortality

    • Family history can reflect inherited biology (lipids, blood pressure regulation, clotting tendency), shared behaviors (diet, smoking, activity), and shared environment.
    • It often shifts disease earlier in life. Earlier disease exposure can increase lifetime risk and can raise overall mortality if not managed.

  4. What studies typically show for family history

    • Having one first-degree relative with premature CVD is linked to higher risk of early CVD (about 1.7–2.2× in the text you provided) and is also associated with higher all-cause mortality.
    • Having two or more affected relatives can signal a much stronger inherited risk (roughly 3.3–5.0× higher early-onset CVD risk in the text you provided).
    • The impact is usually larger when family history is combined with current cardiometabolic risks (high blood pressure, high LDL/ApoB, diabetes, smoking).

Patterns

  • People most affected by a personal CVD history:
    • Those with multiple past events (for example, heart attack plus stroke).
    • Those with heart failure, chronic kidney disease, diabetes, or continued smoking.
    • Those with poor control of blood pressure, LDL/ApoB, and blood sugar after the event.
  • People most affected by family history:
    • Those with premature CVD in a parent or sibling (younger ages at diagnosis are a stronger warning sign).
    • Those with multiple first-degree relatives affected.
    • Those with signs of inherited lipid disorders (very high LDL cholesterol early in life) or early atrial fibrillation in the family.
  • Disparities and environment:
    • The same genetic risk can lead to different outcomes depending on prevention access (screening, medications, follow-up care), affordability, and health literacy.
    • In settings with limited prevention and emergency care, the long-term impact of both personal and family history is often larger.

KamaLama scoring

This factor is scored as an event-based risk signal.

  • Personal CVD history is treated as a major “already happened” event and receives a large negative score.
  • Family history is treated as an inherited-risk signal and receives a smaller negative score.
  • If both apply, the total effect is typically additive across factors in the overall model (each factor contributes its own score).
Category/RangeScore (in years)
Yes-10.0
No0.0
Yes-2.0
No0.0

Practical tips

  • Write down your personal history clearly: event type (heart attack, stroke, heart failure, etc.) and year it happened. Keep it with your medical documents.
  • Record family history for first-degree relatives: which relative, what happened, and the age at first event (especially if young).
  • If you have personal CVD history, focus on the big “mortality levers”: do not smoke, take prescribed medicines consistently, and monitor blood pressure and cholesterol regularly.
  • If you have family history, start prevention earlier: check blood pressure, lipids (LDL and ideally ApoB), blood sugar (HbA1c), and lifestyle risk factors even if you feel well.
  • Build a simple prevention routine: 150 minutes/week of moderate activity (or equivalent), strength training, and a heart-healthy eating pattern you can sustain.
  • Ask your clinician whether your family history suggests inherited conditions (for example familial hypercholesterolemia) that might need earlier or stronger treatment.

References

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