Even if you have a family history of heart problems, you can take steps to prevent a heart attack or stroke, says cardiologist Michael Ozner, MD. Here is his plan to do that…

What Causes Heart Attacks

The root cause of atherosclerotic ­cardiovascular disease (CVD) is excessive cholesterol- and triglyceride-carrying atherogenic lipoproteins in your bloodstream—the result of a flawed lifestyle and/or genetic risk factors. If there are too many of these toxic lipoproteins, they can enter artery walls and, over time, cause a buildup of atherosclerotic plaque—a collection of cholesterol, fats and inflammatory cells. In early stages, plaque is soft, but as you get older, it can harden or calcify. And if plaque becomes highly inflamed, it can rupture, causing a heart attack or stroke.

Even though there are techniques to open blocked coronary arteries and others to remove clots from arteries in the brain to treat stroke, CVD remains the leading cause of death for more than a half million Americans every year. Problem: The medical community tends to wait until a heart attack happens and then spring into action. But for many people, their first symptom is their last…and for those who survive, life is never the same.

It’s time to eliminate the cause of ­atherosclerotic heart disease, says Dr. Ozner. How? By decreasing levels of dangerous lipoproteins beyond what can be achieved with statin medications. Over the last decade, genetic engineering has paved the way for new medications that lead to much lower levels of harmful cholesterol and reverse or shrink dangerous plaque. But it’s up to you to be an informed patient.

Dr. Ozner’s Three-step Plan

Step #1: Get your house in order—meaning your lifestyle. The foundation of heart health is a healthy lifestyle—following the heart-healthy Mediterranean diet, getting regular exercise, lowering stress, maintaining a healthy weight, not smoking and avoiding exposure to air pollution. Double down on your efforts to reach these goals.

Step #2: Find out your plaque status. Visualizing plaques in your arteries and measuring specific components in your blood can provide information about your risk status and guide appropriate treatment.

Imaging tests. The main tests that reveal plaque are…

Computed tomography angiography (CTA)—the optimal imaging test—uses a contrast agent that lights up plaque along the entire coronary artery tree. It can identify not only calcified plaque but also soft plaque, a predictor of future problems. CTA results also can show whether statins and other ­preventive therapies are working.

Coronary artery calcium (CAC) scan measures calcified plaque. A score of zero means no calcium is seen in the heart and suggests a low chance of having a heart attack in the future. When calcium is present, the higher the score, the greater the risk for heart disease. A score of 100 to 300 means moderate plaque deposits. Example: If you have a score of 200 but no symptoms, you can attack plaque with aggressive drug treatment and/or have a CTA to get a more precise picture of your situation. But CAC has a limitation—it can’t identify early soft plaque, which can lead to a heart attack. So you could have a score of 0 and be told not to worry about plaque yet still be at risk. And if your lifestyle isn’t heart-healthy, your score could change in a matter of months or years.

Vascular ultrasound can detect atherosclerotic plaques in peripheral arteries in the legs, thoracic aorta and carotid arteries, though not in the coronary arteries. If plaque is found in these areas, it’s extremely likely to be in the heart arteries as well. Some clinical studies have shown that ultrasound is better at predicting heart attack risk than CAC scans.

Blood tests. To detect risks for CVD, heart attack and stroke, the following tests should be done in addition to standard blood tests such as a complete blood count (CBC), chemistry panel and a lipid profile.

High-sensitivity C-reactive protein (hs-CRP) indicates vascular inflammation. Damage to arteries from fatty deposits and plaque prompts an inflammatory response that causes hs-CRP to rise, along with risk for heart attack and/or stroke. A normal hs-CRP level is under 1.0 mg/L.

Apolipoprotein B-100 (ApoB) is a protein that attaches to potentially harmful lipoproteins, such as LDL. A blood test that measures these particles is a better predictor of heart attack risk than measuring LDL cholesterol alone. A normal level is under 100 mg/dL.

Lipoprotein(a) (Lp(a)) is an LDL particle with a different protein attached (it resembles a little tail). It is more dangerous than run-of-the-mill LDL because it’s linked to increased risk for heart attack, stroke and blood clots. High Lp(a) is a genetic, or inherited, condition and affects up to 20% of people. A high level is 50 mg/dL and above.

Step #3: Personalized heart attack–prevention strategy. Work with your doctor or cardiologist to implement Step #1 and address the findings from Step #2.

Important: Soft plaque deposits can be eradicated with lifestyle changes and medication. Plaques that have calcified can’t be eradicated, but there are treatments to shrink them and reduce dangerous inflammation.

Your prevention strategy should have the following components…

Lower cholesterol. Goal: In people with existing atherosclerotic plaques, getting LDL cholesterol under 50 mg/dL can stabilize or shrink them. For others, maintain LDL cholesterol between 50 mg/dL and 70 mg/dL.

Recent finding: HDL, the so-called good cholesterol, does not necessarily ­correlate with heart disease risk, so the focus has shifted from raising HDL to lowering LDL. Statins have not solved the heart attack epidemic because they lower LDL cholesterol by only about 30%…50% when taken at a high dose. To achieve optimal LDL levels, you might need to reduce your LDL by 70% to 80%. New medications dramatically lower LDL and risk for cardiovascular events. ­Cholesterol-lowering medications available now and on the horizon…

Statins are the first-line medication to lower cholesterol production.

Ezetimibe is a cholesterol absorption inhibitor that has shown to be as effective as monotherapy and when used in conjunction with statin medications.

Bempedoic acid, a prescription medication, also reduces cholesterol production.

PCSK9 inhibitor. PCSK9 is a protein produced in the liver that gets in the way of clearing LDL. When added to statins, a PCSK9 inhibitor helps achieve a further 50% to 60% LDL reduction. PCSK9 inhibitors include evolocumab (Repatha) and alirocumab (Praluent), self-administered by injection every two to four weeks, and inclisiran (Leqvio), given twice a year by a health-care provider.

Pelacarsen significantly lowers Lp(a) and is in a late-stage clinical trial.

Lower triglycerides. Goal: A normal triglyceride level is under 150 mg/dL…an optimal level is under 100 mg/dL. High triglycerides increase heart attack risk. A clinical trial by researchers at Brigham and Women’s Hospital Heart and Vascular Center of Harvard Medical School demonstrated that a highly purified omega-3 EPA ethyl ester (Vascepa) can lower triglycerides by 80%. In a study of people with optimal LDL but whose triglyceride levels were high, by Boston University School of Medicine and other institutions, it lowered cardiovascular risk by more than 25%.

Lower inflammation. Inflammatory cells produce enzymes called proteinases, which can break down the fibrous cap of an atherosclerotic plaque and cause the plaque to rupture. You can lower inflammation with good lifestyle habits and medications, including the gout medication colchicine, if needed.

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