Some of the most consequential cardiovascular diseases develop in people who feel completely well.
They exercise, work demanding jobs, raise families, travel and have no complaints of chest pain.
They may have been told their cholesterol is “normal.” Their blood pressure looks acceptable and may even have passed a stress test.
Then, seemingly out of nowhere, without a warning, cardiovascular disease announces itself, in the form of a heart attack or a stroke or the discovery of advanced coronary atherosclerosis, and in some extreme cases cardiac death.
To the patient and family, the event feels sudden and unannounced, but biologically, that may not be true.
Atherosclerotic cardiovascular disease usually develops over years or decades. Exposure to atherogenic lipoproteins, elevated blood pressure, smoking, diabetes, metabolic dysfunction, inflammation, sedentary behavior, impaired cardiorespiratory fitness, and genetic susceptibility can progressively increase cardiovascular risk long before symptoms develop.
This creates one of the most important questions facing modern cardiology:
If cardiovascular disease develops silently over decades, why does so much of cardiovascular care begin only after symptoms or clinically apparent disease emerge?
I believe the future of heart care needs to evolve towards a precise preventive model.
A model that identifies causal risk early on. Measures cumulative exposure more judiciously. Takes into account the limitations of short-term risk prediction. Detects subclinical disease when clinically appropriate. Intervenes before disease becomes advanced. Measures cardiorespiratory fitness and cardiometabolic health alongside traditional risk factors.
And, perhaps most importantly, tracks whether our interventions are actually working. This is the case for modern preventive cardiology.
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Preventive Cardiology Should Begin With a Simple Biological Reality: Disease Starts Before Symptoms
The first principle of preventive cardiology is straightforward.
The absence of symptoms is not evidence of the absence of disease.
Coronary atherosclerosis develops through the accumulation and retention of ApoB-containing lipoproteins within the arterial wall, followed by complex inflammatory, vascular, and remodeling processes.
This biology begins long before most cardiovascular events occur. The clinical implications are profound.
A person may have hypertension, diabetes, severely elevated LDL cholesterol, elevated lipoprotein(a), impaired cardiorespiratory fitness and coronary atherosclerosis without symptoms.
Symptoms appear late in the biological timeline of cardiovascular disease.
By the time a myocardial infarction, stroke, heart failure hospitalisation, or symptomatic peripheral arterial disease occurs, the opportunity for primary prevention is behind you.
We can still reduce future risk. Secondary prevention is extraordinarily important. But the patient now has established clinical disease.
The central opportunity of preventive cardiology is to deliver meaningful interventions earlier in that timeline to prevent disease.
Cardiovascular events can appear sudden. The disease process that precedes them usually is not.
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Risk Factors Matter. But Risk Factors Are Not the Same as Disease.
Traditional cardiovascular risk assessment has saved lives.
Age, blood pressure, cholesterol, diabetes, smoking, kidney disease, and other variables allow clinicians to estimate the probability of future cardiovascular events.
Contemporary tools such as the American Heart Association PREVENT equations represent an important evolution in risk assessment by incorporating cardiovascular, kidney, and metabolic health and estimating both 10-year and 30-year risk.
Risk estimation is fundamental to prevention. But every model has limitations. A risk calculator estimates probability within populations. It is not personalized, it does not directly measure whether an individual has coronary atherosclerosis. It does not quantify a lifetime of prior exposure to elevated ApoB-containing particles. It may not fully capture family history, lipoprotein(a), ethnicity-related risk, cardiorespiratory fitness, or other clinically important factors in every patient.
And short-term risk can sometimes be misleading in younger adults.
A 42-year-old individual may have a relatively low calculated 10-year risk largely because of age, but when one looks at their lifetime exposure to hypertension, diabetes, elevated ApoB, smoking, severe obesity, elevated Lp(a), or a strong family history of premature coronary disease, the risk definition may change.
This is why preventive cardiology cannot stop at a single risk score.
Risk estimation should be the beginning of a clinical conversation, not necessarily the end of one.
Risk factors estimate probability. They do not always tell us whether disease is already present.
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The Future of Prevention Requires Greater Attention to Cumulative Exposure
One of the most important developments in cardiovascular science is a more in-depth understanding of cumulative exposure. LDL cholesterol is a useful example.
The cardiovascular consequences of atherogenic lipoproteins are influenced not simply by a single measurement obtained during a yearly physical, but by the magnitude and duration of exposure over time.
The arterial wall is subject to years of biological exposure. The same principle applies to other cardiovascular risks. Blood pressure burden accumulates. Hyperglycemia and metabolic dysfunction accumulate. Smoking exposure accumulates. Sedentary behavior accumulates.
The consequences of poor cardiorespiratory fitness amass. This has major implications for prevention.
Waiting until a patient crosses an arbitrary short-term risk threshold can mean losing years during which modifiable risk could have been addressed.
Earlier identification does not necessarily mean earlier medication for everyone. It means earlier recognition, lifestyle intervention, and treatment when the expected benefits justify it.
And a better understanding of the difference between 10-year event probability and lifetime cardiovascular exposure.
The question should not simply be: “What is this patient’s risk today?”
We should also ask: “What biological exposures are accumulating, and what will happen if they continue for another 10, 20, or 30 years?”
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Prevention Must Move Beyond LDL Cholesterol Alone
LDL cholesterol stays a foundation of cardiovascular risk assessment and treatment. But LDL-C tells only part of the story of the atherogenic lipoprotein burden.
Atherosclerosis is driven by ApoB-containing lipoproteins, including LDL particles, very-low-density lipoprotein remnants, intermediate-density lipoproteins, and lipoprotein(a).
Each atherogenic particle contains one ApoB molecule. ApoB therefore provides an estimate of the number of circulating atherogenic particles.
This distinction becomes important especially when LDL-C and particle number are conflicting, which can occur in individuals with diabetes, hypertriglyceridemia, insulin resistance, metabolic syndrome, and obesity.
Lipoprotein(a), or Lp(a), adds yet another dimension. Lp(a) is predominantly genetically determined and causally connected with atherosclerotic cardiovascular disease and calcific aortic valve disease.
Individuals with significantly high Lp(a) often remain unaware of it because it is not routinely measured in annual tests.
The 2026 multisociety dyslipidemia guideline underlines the importance of early identification and treatment of lipid-related risk, including once-in-adulthood measurement of Lp(a) and selective use of ApoB to refine risk assessment. This is an important evolution.
But biomarkers must be used wisely. More testing does not automatically lead to better medicine.
The purpose of measuring ApoB or Lp(a) is to answer a clinical question and, when appropriate, change management.
The best biomarker is not the newest test. It is the measurement that meaningfully improves a clinical decision.
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We Must Distinguish Risk Prediction From Disease Detection
This may be one of the most important conceptual distinctions in preventive cardiology. Risk factors estimate the probability of disease and future events. Imaging can, in selected circumstances, identify evidence of disease itself.
Coronary artery calcium scoring is one such example. CAC scoring can improve risk classification in selected asymptomatic adults when uncertainty remains about preventive treatment decisions.
The presence and burden of coronary calcium provide evidence of coronary atherosclerosis and can meaningfully reclassify risk.
But CAC has limitations. It detects calcified plaque. It does not directly visualize noncalcified coronary plaque, characterize stenosis, or provide comprehensive assessment of coronary anatomy.
Coronary CT angiography can identify calcified and noncalcified plaque, coronary stenosis, and selected high-risk plaque characteristics. Quantitative CCTA technologies are increasingly capable of characterizing plaque burden and composition.
This is scientifically compelling. But scientific capability must not be confused with evidence supporting population-wide screening. Current evidence does not support performing coronary CTA in every asymptomatic adult.
There are important questions to consider when recommending this test: radiation exposure, contrast administration, incidental findings, downstream testing, cost-effectiveness, overdiagnosis, and most importantly, whether CCTA screening strategies improve cardiovascular outcomes beyond aggressive risk-factor management.
Ongoing randomized trials may shed clarity on some of these questions. The right approach would be neither to dismiss advanced imaging nor to promote indiscriminate screening.
It is to ask: In which carefully selected patients will identifying subclinical disease meaningfully change management?
That is a far more clinically useful question.
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A Normal Stress Test Is Not a Certificate of Arterial Health
One misunderstanding I encounter repeatedly is the belief that a normal stress test means the coronary arteries are free of atherosclerosis. That is not what most stress tests are designed to determine.
Stress testing primarily evaluates the physiological consequences of coronary disease, particularly whether blood flow becomes inadequate under stress.
Coronary atherosclerosis can exist without producing inducible myocardial ischemia. A patient may therefore have coronary plaque despite a normal stress test. This does not make stress testing unimportant.
It means different tests answer different clinical questions. A stress test may ask:
CAC scoring asks: Is there evidence of inducible ischemia?
CTA scoring asks: Is calcified coronary atherosclerosis present, and what is its burden? What does the coronary anatomy look like? Is plaque present? What is the plaque burden and composition? Is there stenosis?
The correct test depends on the patient and the clinical question.
A normal stress test does not answer the same question as a test designed to identify coronary plaque.
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Modern Prevention Must Treat Cardiometabolic Health as Cardiovascular Medicine
Cardiovascular prevention and metabolic health are intricately linked; we cannot talk of one without mentioning the other.
Insulin resistance, hypertension, visceral adiposity, dyslipidemia, chronic kidney disease, physical inactivity, poor diet quality, sleep disorders, and diabetes interact to accelerate cardiovascular risk.
Despite that, each condition is treated by a separate speciality in healthcare. The cardiologist manages cholesterol. The primary care physician manages blood pressure. The endocrinologist manages diabetes. The dietitian addresses nutrition. The trainer manages exercise.
Each professional may provide excellent care. But cardiovascular risk is the integrated result of the entire biological system. Modern preventive cardiology should help connect these domains.
This means moving beyond a narrow focus on whether LDL cholesterol is “normal.” We should also consider:
Blood pressure control | Atherogenic particle burden | Glycemic health |Kidney function | Body composition | Visceral adiposity |Smoking exposure | Sleep | Nutrition quality | Physical activity |Muscular strength | Cardiorespiratory fitness.
The goal is not to order every available test, but characterize the major modifiable determinants of cardiovascular risk accurately enough to intervene intelligently.
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Cardiorespiratory Fitness Deserves a Larger Role in Cardiovascular Prevention
If there is one major cardiovascular risk marker that remains underused in routine clinical medicine, it is cardiorespiratory fitness.
The evidence linking cardiorespiratory fitness with cardiovascular outcomes and mortality is substantial.
The American Heart Association has argued that cardiorespiratory fitness should be considered a clinical vital sign.
A 2024 overview of meta-analyses representing more than 20.9 million observations found strong and consistent inverse associations between cardiorespiratory fitness and mortality and incident chronic disease. Yet most adults have never had their fitness objectively measured.
This is a missed opportunity.
VO₂ max, measured during cardiopulmonary exercise testing, provides an integrated assessment of the cardiovascular, pulmonary, circulatory, and muscular systems’ ability to transport and utilize oxygen during exercise.
But measuring fitness is only the beginning. The more important question is whether we can improve it.
Exercise is one of the most powerful interventions available for improving cardiovascular health, metabolic function, physical capacity, and healthy aging.
Preventive cardiology should therefore move beyond asking: “Do you exercise?”
We should increasingly ask: “What is your cardiorespiratory fitness, what factors are limiting it, and is your training program improving it?”
Exercise is a behavior. Cardiorespiratory fitness is a measurable physiological characteristic. We should pay attention to both.
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Prevention Without Measurement Becomes Guesswork
Modern medicine measures disease such as ejection fraction in heart failure, tumor size in oncology, viral load in infectious disease or haemoglobin A1c in diabetes.
But prevention is often treated differently. It’s generically advised. For instance a patient is told to exercise, eat better, lose weight, lower cholesterol, and improve blood pressure.
Then months pass. The central question becomes:
Did the intervention work?
Did ApoB decrease? Was blood pressure controlled outside the physician’s office? Did glycemic health improve? Did visceral adiposity decrease? Did cardiorespiratory fitness increase? Did the patient become stronger? Did medication adherence improve? Did tobacco exposure stop? Did sleep improve? Did the intervention produce a meaningful change in the biological variable we were trying to modify?
This is where longitudinal preventive care becomes powerful.
Measure. Intervene. Reassess. Adjust.
Prevention should be treated as an ongoing clinical process rather than a single annual conversation.
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Precision Prevention Does Not Mean Maximum Testing
There is an important danger in the emerging preventive-health and longevity industries.
The pendulum can swing too far.
More biomarkers. More imaging. More wearables. More scans. More supplements. More interventions. More data.
But data without clinical context can create anxiety, incidental findings, false positives, unnecessary procedures, financial burden, and overtreatment.
Precision prevention should not mean maximalist medicine.
It should mean asking better questions such as:
What is this patient’s baseline risk?
What risk enhancers are present?
What information is missing?
Would obtaining that information change management?
What are the potential harms of testing?
What interventions have evidence for improving outcomes?
What should we measure longitudinally?
What is uncertain?
An intellectually honest preventive cardiologist must be willing to say both: “We should look deeper.” and “This test is unlikely to help you.”
Those positions are not contradictory. They are both essential to evidence-based care.
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The Future of Prevention Must Be Personalized Without Abandoning Guidelines
Guidelines are indispensable. They integrate evidence, help standardize care, and reduce inappropriate variation, thereby improving outcomes.
But guidelines are designed for populations. Physicians care for individuals.
The practice of medicine exists in the space between population-level evidence and patient-level decision-making.
Two 45-year-old patients may have identical LDL cholesterol values but very different cardiovascular risk.
One may have no family history, normal blood pressure, excellent cardiorespiratory fitness, no diabetes, and no additional risk enhancers.
The other may have South Asian ancestry, a father who experienced a myocardial infarction at 48, elevated Lp(a), hypertension, visceral adiposity, insulin resistance, and poor cardiorespiratory fitness.
Treating these patients identically because a single laboratory value is the same would overlook clinically important differences.
Personalization does not mean ignoring guidelines.
It means using guidelines as the foundation while incorporating individual risk, patient preferences, risk enhancers, comorbidities, family history, and in selected circumstances, additional testing.
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The Future of Heart Care Should Begin Earlier
For much of modern cardiology, our greatest technological achievements have occurred at the end of the cardiovascular disease timeline.
We can open an occluded coronary artery during a heart attack, replace diseased heart valves through catheters, or implant defibrillators capable of terminating lethal arrhythmias or provide mechanical circulatory support to a failing heart.
These achievements are extraordinary. We should continue advancing them.
But the next great frontier of cardiovascular medicine may be earlier. Before the heart attack or the stroke or symptomatic heart failure or advanced vascular disease or decades of cumulative biological exposure become irreversible clinical disease.
This approach requires a different mindset.
It requires identifying risk earlier. Understanding lifetime exposure. Treating causal risk factors appropriately. Using advanced biomarkers selectively. Detecting subclinical disease when the information is likely to change management. Measuring cardiometabolic health. Measuring cardiorespiratory fitness. Building sustainable exercise, nutrition, sleep, and lifestyle strategies. Using pharmacologic therapy when evidence and expected benefit justify it.
Track outcomes and then:
Reassess | Adjust | Repeat.
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What This Means for You
If you are an adult interested in preventing cardiovascular disease, the route is not to go out there and demand every advanced test available.
Start with fundamentals. Know your blood pressure. Understand your lipid profile. Discuss whether ApoB or Lp(a) measurement would add useful information.
Know your family history, particularly premature cardiovascular disease. Assess for diabetes, kidney disease, smoking exposure, obesity, metabolic dysfunction, and other major risk factors.
Exercise regularly. Build and preserve muscle. Improve cardiorespiratory fitness. Prioritize dietary quality. Sleep adequately. And do not smoke.
Work with a clinician to estimate both near-term and longer-term cardiovascular risk. If uncertainty remains, discuss whether additional risk stratification, such as coronary artery calcium scoring or other individualized testing, is appropriate.
The objective is not more testing. The objective is better information that leads to better decisions.
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The Pulse Perfect Approach: From Episodic Care to Longitudinal Cardiovascular Optimization
I created Pulse Perfect, Cardiovascular Optimization & Longevity around a simple observation.
Many people want to better understand their cardiovascular health before they develop symptomatic disease.
Traditional cardiology is exceptionally good at evaluating symptoms, diagnosing cardiovascular disease, performing procedures, and managing established illness.
Pulse Perfect is designed to complement that system.
Our approach goes beyond routine heart check-ups. We take a comprehensive look at your cardiovascular health, identify the risk factors you can control, and use advanced heart tests and biomarkers only when they are truly needed.
We also evaluate your cardiometabolic health and fitness levels, then create a personalized plan tailored to your goals. Most importantly, we track your progress over time, assess and adjust to help you build and maintain better heart health for the long term.
The goal is not to perform every available test but to ask better questions.
What is driving this individual’s cardiovascular risk?
Is there evidence of subclinical disease that would meaningfully change management?
Which modifiable variables matter most?
What interventions are supported by evidence?
How will we measure whether those interventions are working?
And what can we do today that may meaningfully change cardiovascular health over the next several decades?
Conclusion: A Manifesto for the Next Era of Heart Care
The future of cardiology cannot be defined only by our ability to rescue patients from advanced cardiovascular disease.
It must also be defined by our ability to prevent more people from reaching that point. That requires earlier recognition of risk. Greater attention to cumulative exposure. More precise measurement of atherogenic lipoproteins and cardiometabolic health. Appropriate detection of subclinical disease in selected patients. Greater attention to cardiorespiratory fitness. Intelligent use of technology. Longitudinal measurement. Clinical restraint when testing is unlikely to improve decisions.
And a willingness to acknowledge uncertainty where evidence remains incomplete.
Preventive cardiology should not become a competition to order the most tests.
It should become the discipline of obtaining the right information, in the right patient, at the right time—and using that information to change the trajectory of cardiovascular health.
The most important question in heart care should not always be: “How do we treat cardiovascular disease once it becomes clinically apparent?”
Increasingly, we should also ask: “How early can we identify meaningful risk, how intelligently can we intervene, and how many cardiovascular events can we prevent before symptoms ever begin?”
That is the future of preventive cardiology.
And that future begins before symptoms.
Frequently Asked Questions
Q: Can you have heart disease without symptoms?
A: Yes. Hypertension, diabetes, lipid disorders, and coronary atherosclerosis may remain asymptomatic for years. The absence of symptoms does not rule out cardiovascular risk or subclinical disease.
Q: Should every healthy adult undergo coronary CTA?
A: No. Current evidence does not support population-wide CCTA screening of asymptomatic adults. CCTA may provide important anatomical and plaque information, but its use will depend from patient to patient depending on their clinical risk, the question being asked, potential harms, and whether the result is likely to change management.
What is the difference between a risk calculator and cardiovascular imaging?
A: Risk calculators help estimate the likelihood of future cardiovascular events using population-derived clinical variables. Cardiovascular imaging, on the other hand, detects evidence of whether the disease already exists, depending on the modality used. Risk prediction and disease detection answer related but different questions.
Q: Is ApoB better than LDL cholesterol?
A: ApoB estimates the number of circulating atherogenic lipoprotein particles, while LDL-C measures the cholesterol mass carried within LDL particles. ApoB can provide additional information when LDL-C and particle burden are discordant, particularly in people with hypertriglyceridemia, diabetes, obesity, or metabolic dysfunction.
Q: Why is cardiorespiratory fitness important?
A: Cardiorespiratory fitness reflects the integrated ability of the cardiovascular, pulmonary, circulatory, and muscular systems to deliver and utilize oxygen during physical activity. Higher fitness is strongly associated with lower cardiovascular and all-cause mortality risk, although much of this evidence is observational.
Q: What is the first step toward a more proactive approach to cardiovascular prevention?
A: The first step in a proactive approach to cardiovascular disease is accurately describing established risk factors: blood pressure, lipid levels, diabetes status, smoking exposure, kidney health, family history, physical activity, body composition. Additional biomarkers or imaging should be considered selectively when they are likely to improve clinical decision-making.
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