Beyond Blockages: Can Atherosclerosis and Stable Angina Be Stabilized, or Even Reversed—Without Stents or Bypass Surgery?
Here are my answers and discussions for those who suffers from coronary heart disease and who cares and values what I write
by lim ju boo, alias lin ru wu (林 如 武)
Atherosclerosis, the progressive buildup of lipid-rich plaques within the walls of arteries, lies at the heart of coronary artery disease (CAD), stroke, and peripheral vascular disease. For decades, it was regarded as an inexorably progressive condition, one that could be bypassed or mechanically opened but never truly altered. This view has changed substantially. Modern cardiovascular science now recognizes atherosclerosis as a dynamic biological process, one that can be slowed, stabilized, and in selected circumstances partially reversed, provided intervention is sufficiently early, sustained, and comprehensive.
The Biology of Atherosclerosis: Can Plaques Really Regress?
Atherosclerosis is fundamentally an inflammatory disease driven by the accumulation of low-density lipoprotein (LDL) cholesterol within the arterial wall. LDL particles penetrate a damaged endothelium, become oxidized, and trigger an inflammatory cascade involving macrophages, foam cells, smooth muscle proliferation, and extracellular lipid deposition. Over time, this process forms plaques that narrow arteries and compromise blood flow.
Although atherosclerosis remains a chronic condition, it is no longer correct to say it is entirely irreversible. Imaging studies using intravascular ultrasound (IVUS) and coronary CT angiography have demonstrated that intensive lipid-lowering therapy, particularly with high-dose statins and newer agents, can produce modest but measurable reductions in plaque volume, typically in the range of 1–5% over one to two years. While this degree of shrinkage may appear small, its clinical impact can be significant.
More important than plaque size reduction is plaque stabilization. Intensive therapy transforms plaques from soft, lipid-rich, rupture-prone structures into more fibrotic, stable lesions with thicker caps. Since most heart attacks result not from gradual narrowing but from sudden plaque rupture followed by thrombosis, stabilization dramatically reduces the risk of catastrophic events even when angiographic stenosis remains unchanged.
The stage of disease is crucial. Early, lipid-rich plaques respond far better to intervention than advanced, heavily calcified lesions. Once calcification dominates, true regression becomes difficult, though stabilization remains achievable.
Lowering Risk Aggressively: Medical and Lifestyle Foundations
To achieve plaque stabilization or regression, cardiovascular risk factors must be managed aggressively, often aiming for LDL cholesterol levels below 70 mg/dL, and in very high-risk patients, below 50 mg/dL.
Statins remain the cornerstone of therapy. High-intensity statins such as atorvastatin and rosuvastatin lower LDL cholesterol, reduce vascular inflammation, and stabilise plaques. When statins alone are insufficient or poorly tolerated, ezetimibe can further reduce intestinal cholesterol absorption, and PCSK9 inhibitors, powerful injectable agents, can lower LDL dramatically, with studies showing plaque regression in a substantial proportion of patients.
Lifestyle modification is not an adjunct but a biological intervention. Very low-fat, whole-food, plant-based diets, such as those studied by Ornish and others, have demonstrated regression of coronary disease in selected patients.
Besides nutrition and dietary changes other lifestyle modifications need to be addressed.
If you smoke, stop at once or at least gradually. Quitting smoking is considered the most powerful and cost-effective step for protecting the heart. Tobacco toxins cause direct endothelial damage, promote plaque buildup, and increase the risk of blood clots. This includes avoiding vaping and secondhand smoke, both of which trigger arterial inflammation.
Smoking cessation is immediate and critical; it halts ongoing endothelial injury and reduces thrombogenicity within weeks.
Regular physical activity comes next. Aim for at least 150–300 minutes of moderate-intensity aerobic exercise (e.g., brisk walking, cycling, swimming) or 75–150 minutes of vigorous activity per week. Exercise helps stabilize plaques by reducing the lipid core and thickening the fibrous cap, making them less prone to rupture.
High volumes of aerobic exercise improve endothelial function, insulin sensitivity, and lipid metabolism. However, do NOT engage in excessive, prolonged, and strenuous exercises if you know you already already suffering from coronary heart disease and angina pectoris (chest pains). You may suddenly collapse from an AMI (acute myocardial infraction or heart attack), or even a total cardiac arrest from cardiac electrical transmission failure. See my explanation here:
https://scientificlogic.blogspot.com/search?q=jogging+and+exercise
If you are obese or overweight weight management is crucial. Losing even 5–10% of body weight can significantly improve cholesterol and blood pressure levels. Reducing central obesity (waist circumference) is particularly important as visceral fat has a direct link to plaque formation.
Consider stress management. Chronic mental stress can double the risk of heart attacks by increasing blood pressure and triggering inflammatory responses. Effective techniques include mindfulness, meditation, deep breathing (e.g., the 4-7-8 method), and cognitive behavioral therapy.
Optimal sleep hygiene is another helpful factor. Aim for 7–9 hours of quality sleep per night. Inadequate sleep (≤4 hours) or excessive sleep (≥10 hours) is associated with an increased risk of coronary artery disease.
If you drink, limit alcohol intake. While some studies previously suggested benefits for red wine, 2026 health guidelines increasingly emphasize that any amount of alcohol may increase atherosclerotic risk. If consumed, limit to no more than one drink daily for women and two for men.
Regular health checkups is useful. Schedule annual physicals to monitor "silent" risk factors like blood pressure, cholesterol, blood sugar (A1c). Early detection allows for intervention before plagues become unstable.
Ensure strict control of underlying conditions.
Actively managing diabetes and hypertension is essential, as these conditions significantly accelerates plague hardening and progression
Stable Angina: A Symptom, Not a Sentence
Stable angina represents the most common clinical manifestation of CAD. It is characterized by predictable chest discomfort arising when myocardial oxygen demand exceeds supply, typically during exertion, emotional stress, heavy meals, or exposure to cold. The pain is usually brief, lasting less than five minutes, and resolves with rest or nitroglycerin. It is often described as pressure, tightness, or heaviness rather than sharp pain, and may radiate to the arms, neck, jaw, or back. Importantly, certain groups, particularly women, older adults, and individuals with diabetes, may present with atypical symptoms such as breathlessness, nausea, or profound fatigue. Stable angina is usually caused by fixed, stable plaques that limit coronary flow during increased demand rather than by acute plaque rupture. Its predictability distinguishes it from unstable angina, which signals imminent risk of myocardial infarction and requires urgent evaluation. While stable angina is manageable, it is not benign. Any change in pattern such as pain at rest, prolonged discomfort, lack of response to nitrates, or increased severity, should prompt immediate medical attention.
Whether stable angina can be managed without angioplasty or coronary artery bypass grafting (CABG) depends largely on the extent, location, and physiological impact of coronary stenosis, a discussion that must be individualized.
Blood Thinners: Protection Without Plaque Removal
The term “blood thinners” is commonly misunderstood. It refers broadly to two distinct classes of medication: anticoagulants and antiplatelets.
Anticoagulants, including direct oral anticoagulants such as apixaban, rivaroxaban, dabigatran, and edoxaban, as well as warfarin and injectable heparins, interfere with the clotting cascade. Antiplatelet agents such as aspirin, clopidogrel, ticagrelor, and prasugrel prevent platelets from aggregating at sites of vascular injury.
These drugs do not thin the blood, nor do they prevent or reverse atherosclerosis. Their role is to prevent clot formation on top of existing plaques, especially when plaques rupture or endothelial surfaces become thrombogenic. This is why they reduce the risk of heart attacks and strokes without altering plaque burden.
Medications that truly modify plaque biology are lipid-lowering and anti-inflammatory agents, most notably statins and their adjuncts. Blood thinners are protective but not curative, and they cannot substitute for revascularisation when severe flow-limiting disease is present.
Nutrition and Diet is Exceedingly Important in Preventive and Curative Medicine: Can Food Stabilize or Reverse Disease?
By 2026, clinical consensus increasingly supports a “portfolio approach” to lipid management, combining multiple foods and nutrients that act through different mechanisms to improve cholesterol profiles and vascular health.
In tropical countries like Malaysia, nature offers a rich array of fruits and vegetables high in soluble fibre, antioxidants, and phytochemicals. These compounds reduce cholesterol absorption, improve bile excretion, dampen inflammation, and enhance endothelial function.
Avocados, rich in monounsaturated fats and fibre, have demonstrated the ability to lower LDL cholesterol while modestly raising HDL cholesterol in controlled studies. Guava provides abundant pectin and vitamin C, supporting cholesterol excretion and antioxidant defence. Mangoes contribute fibre and polyphenols that reduce dietary cholesterol absorption. Vegetables like lady's fingers and brinjals bind bile acids in the gut, while water spinach (kangkong) supplies antioxidants and potassium that support blood pressure regulation. Emerging research suggests that the leaves of the miracle fruit may possess lipid-lowering properties, though further study is needed.
What about drinking green and oolong teas? While both teas come from the Camellia sinensis plant, they undergo different processing that affects their specific bioactive compounds. Green tea is highly effective at reducing total and LDL ("bad") cholesterol due to its high concentration of catechins, specifically epigallocatechin gallate (EGCG). Catechins inhibit the absorption of dietary cholesterol in the intestines and promote its excretion. Studies show green tea can reduce total cholesterol by 5–10%. although most research indicates green tea has little to no significant effect on HDL ("good") cholesterol or triglycerides Consuming 2–4 cups daily or supplements with at least 150 mg of catechins is often recommended for optimization.
Oolong tea is partially fermented, giving it a unique profile of both green tea catechins and black tea's polymerized polyphenols. It contains oolong tea polymerized polyphenols (OTPP), which are thought to inhibit pancreatic lipase, the enzyme that digests fats, thereby preventing fat absorption. Regular long-term consumption has been associated with significant reductions in total cholesterol, LDL, and notably, triglycerides (up to nearly 12% in some long-term studies).
Drinking at least 10 ounces (roughly 1.5 cups) per week or 1 cup daily has been linked to lower risks of high cholesterol. Best for LDL: Green tea typically shows a stronger direct effect on lowering LDL cholesterol compared to oolong.
Oolong tea may be more effective than green tea at managing triglyceride levels.
For maximum benefit, brew tea at high temperatures (over 80°C / 176°F) for at least 3–5 minutes to ensure full extraction of polyphenols.
However, tea contains caffeine, which may slightly raise blood pressure in sensitive individuals. It can also interfere with certain medications, such as statins or beta-blockers.
Beyond whole foods, certain supplements provide concentrated doses of bio-active compounds. Niacin (vitamin B3) remains one of the most effective agents for raising HDL cholesterol while lowering LDL and triglycerides, though high doses require caution. Omega-3 fatty acids from fish oil or its supplements primarily reduce triglycerides and exert anti-inflammatory effects. I recommend frequent consumption of salmon, mackerel. herring and trout that are very rich in heart-protective EPA and DHA.
Plant sterols and stanols block intestinal cholesterol absorption and can lower LDL by approximately 10% when taken at adequate doses. Plant sterols and stanols are naturally found in vegetable oils, nuts, seeds, whole grains, fruits and vegetables, but in small amounts; for therapeutic cholesterol lowering. Look for foods fortified with them, like some yogurts, spreads, orange juice, and cereal bars, which have significantly higher effective doses.
Red yeast rice contains monacolin K, chemically identical to statins, and can significantly lower LDL cholesterol. Psyllium husk provides potent soluble fibre, while berberine may reduce both LDL cholesterol and triglycerides.
Other core heart-healthy foods besides oily fish, are extra virgin olive oil rich in polyphenols, nuts containing healthy fats and phytosterols, whole grains rich in beta-glucan, and deeply pigmented purple fruits and vegetables high in anthocyanins.
Dietary and nutritional strategies do not mechanically remove plaques. Their benefit lies in lowering LDL cholesterol, reducing inflammation, improving endothelial function, and stabilizing existing plaques. In carefully selected patients, such approaches, when combined with medication, may delay invasive procedures such as angioplasty or even open-heart by-pass surgery (CABG) . However, dietary approaches alone cannot universally replace angioplasty or bypass surgery, particularly in advanced multi-vessel disease with critical stenosis.
It is essential to note that some supplements, including red yeast rice and high-dose niacin, can cause adverse effects or interact with prescribed medications. Medical supervision is always advised.
Revascularisation: Treating Flow, Not Disease
Angioplasty with stenting and coronary artery bypass surgery remain powerful tools for restoring blood flow in critically narrowed vessels. However, they do not cure atherosclerosis. They treat focal obstructions while leaving the underlying systemic disease intact. Long-term outcomes, therefore, still depend on aggressive risk factor modification, medical therapy, and lifestyle change.
Let me summarize what I have explained and written:
Atherosclerosis is no longer a hopelessly progressive disease. It is a modifiable biological process. Stable angina is not an automatic sentence to the catheterization lab or operating theater. Through intensive lipid lowering, appropriate medications, disciplined lifestyle change, and evidence-based nutrition, many patients can stabilize their disease and significantly reduce their risk of heart attack and death.
But it also is exceedingly important to note that it does not mean after angioplasty or a coronary bypass surgery all the problems is solved permanently without any need to change our dietary lifestyles and other lifestyles such as continue to eat what we like, continue to be obese and overweight, continue to consume a lot of sugar, or continue to smoke or live aggressively with unnecessary anger and unnecessary stress, in which case the same heart problem will return, and nothing else, whether medical or surgical can be done after that. Note this well written in red. .
Nevertheless, medicine must remain honest. Not all plaques regress. Not all patients can avoid procedures. The art of cardiovascular care lies in matching the right patient to the right intervention at the right time, guided by science, compassion, and humility.
Selected References for Further Reading
1. Nissen SE et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N Engl J Med.
2. Nicholls SJ et al. Effect of intensive lipid lowering on coronary atherosclerosis. JAMA.
3. Sabatine MS et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med.
4. Ornish D et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA.
5. Stone NJ et al. 2018 AHA/ACC Guideline on the Management of Blood Cholesterol. Circulation.
6. Libby P. Inflammation in atherosclerosis. Nature.
7. Yusuf S et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med.
