16
In the preceding pages I have taken you on a guided tour of how America’s epidemiologic transition of the early 20th century brought a steep rise in mortality due to atherosclerotic heart disease and how the medical advances in many disciplines during the past six decades have helped us turn the curve and bring cardiovascular mortality down to levels well below what they were in 1900. From a health care consumer’s perspective, here are the practices that will minimize your risk of suffering and dying from atherosclerotic cardiovascular event:
1. If you have no cardiovascular disease or risk factors:
• Don’t smoke cigarettes. As an added bonus, you will also minimize your risk of dying from respiratory (and some non-respiratory) cancers and other lung diseases.
• Don’t eat more calories than you can burn. Avoid caloric fatty snacks and sugary drinks, and exercise regularly.
• Types of food: Get your calories from fresh fruits and vegetables, whole grains, and unsaturated vegetable oils. Minimize saturated fats and salt.
2. If you have cardiovascular risk factors, you should also:
• Lower your blood pressure to < 130/80 mmHg. Thiazide diuretics, ACE inhibitors (and angiotensin receptor blockers), calcium channel blockers, and (to a lesser extent) beta blockers are safe and effective antihypertensive drugs.
• Lower your LDL cholesterol to < 130 mg/dL—or to <100 mg/dL if you have atherosclerotic cardiovascular disease, diabetes, or other risk factors. Statins are the drug of choice.
• If you smoke cigarettes, stop.
3. If you are experiencing the symptoms of a heart attack, you should receive urgent medical attention to include:
• Cardiopulmonary resuscitation (CPR) if there is no heartbeat.
• Coronary angiography and stent placement to open up acutely blocked coronary arteries.
• Aspirin and other antiplatelet drugs to prevent stent thrombosis.
• If a cardiac catheterization lab is unavailable, intravenous thrombolytic therapy is a viable alternative.
4. If you have had a heart attack in the past and/or have symptoms of advanced atherosclerotic heart disease, you should:
• Take a statin, aspirin, an ACE inhibitor, and a beta blocker, whether or not you have specific indications (high LDL cholesterol, hypertension, heart failure) for those drugs.
• If you have angina or other signs of cardiac ischemia, get evaluated by coronary angiography and consider coronary artery bypass surgery (CABG) if your left main coronary artery is significantly obstructed. The internal thoracic artery is superior to venous grafts as a conduit.
• If you are at high risk for sudden cardiac arrest due to a known ventricular arrhythmia or significant ventricular dysfunction, consider an implantable cardioverter defibrillator (ICD).
The impact of an intervention on the public health depends not only on its efficacy when it is implemented, but on how broadly and well it is implemented. The first set of recommendations, for what is sometimes called “primordial prevention,” is aimed to prevent the emergence of cardiovascular risk factors like high BP, high LDL cholesterol, smoking, obesity, and diabetes by promoting a healthy lifestyle starting in childhood. In theory, this should have been the keystone of our efforts to reverse the rise of cardiovascular mortality in the first half of the 20th century, since adverse population changes in diet, physical activity, and cigarette smoking are what caused it in the first place. Unfortunately, the U.S. population as a whole has continued to grow fatter and more sedentary, and the rise in our prevalence of type 2 diabetes has accelerated.
From a public heath perspective, our crowning achievement has been our success in implementing the second set of interventions, for primary prevention. Although the impact of these treatments is delayed and undramatic, more than half of all American adults had one or more of these risk factors when heart attack mortality peaked in the 1960s. The third set of recommendations, which are aimed at increasing survival of an acute life-threatening coronary artery blockage or arrhythmia, are the most dramatic and spectacular, but their impact has been limited by the stubborn reality that many of these patients die before any medical help can arrive. The fourth set of recommendations, for secondary prevention, though quite successful, has also been limited by the fact that they are applicable only to survivors of an acute MI. Thus, although high-tech interventions like CPR, ICD placement, and coronary revascularization may be dramatically and immediately beneficial in those who receive them, it is the less dramatic but more sustainable low-tech interventions for controlling BP, LDL cholesterol and cigarette smoking that have made the biggest difference.
I have attempted to parse out the relative contributions of the major advances of the past 50 years to the 81% decline in heart attack mortality since 1968.
• I attribute 55.7% of the decline to primary prevention—specifically, cholesterol lowering (mainly statins), treatment of hypertension, and smoking cessation, in that order—perhaps, with a 2–3% offset for the rising prevalence of type 2 diabetes,
• I attribute 13.7% of the decline to advances in the treatment of acute myocardial infarction (mainly to urgent angioplasty and stent placement in conjunction with anti-platelet drugs) and perhaps 2–5% to other acute interventions
• I attribute 23.3% of the decline to secondary prevention in MI survivors—specifically, statins, aspirin, RAAS inhibitors (mostly ACE inhibitors), and beta blockers, in that order.
Of course, these are only estimates, relying on many assumptions and approximations. Since these interventions apply to different patient populations, their estimated contributions to the decline in heart attack mortality may be combined by simple addition. Although they do not quite add up to 100%, some of these figures may underestimate the true impact of these trends for reasons explained in the preceding chapters.
You may notice that there is a natural hierarchy in the four groups of recommendations I have presented. In the best of all worlds, people would adopt and sustain a healthy lifestyle that would keep them fit and healthy and would obviate much of the need for primary prevention drugs. Unfortunately, human nature being what it is, nothing short of poverty, war, and famine have curbed on our growing tendency toward dietary excess over the past century. Given the draconian nature of these “cures,” we have successfully pursued primary prevention as a fallback plan to mitigate the harm done by unhealthful lifestyle choices. When primary prevention fails and a myocardial infarction or arrhythmia occurs, acute intervention followed by secondary prevention in the survivors is the final fallback. But our success in primary prevention, which has prevented 45% of the heart attacks that would have happened in 1968 from happening in 2017 has limited the scope and impact of these secondary strategies. Just as our lack of success in primordial prevention has amplified the need for primary prevention, our success in primary prevention has lessened the need for acute and secondary intervention. If our primary prevention efforts had prevented only 10% of heart attacks, acute and secondary interventions would have assumed a far greater significance.
While the four sets of recommendations listed above demonstrably save lives, many other cardiac interventions are also useful even if they have not been proven to prevent heart attack deaths. For example, a wide selection of drugs is available to control blood glucose and HbA1C levels in type 2 diabetes and thereby reduce microvascular complications like blindness, neuropathy, and kidney failure. Oral nitrates and non-urgent angioplasty and stent placement can alleviate angina symptoms and improve quality of life. Judicious use of estrogen therapy can alleviate vasomotor and other debilitating symptoms following menopause, especially in women whose ovaries have been surgically removed. Other once promising interventions, like CETP inhibitors to raise HDL cholesterol and certain anti-arrhythmic drugs, have turned out to be useless or worse.
I have focused primarily on atherosclerotic coronary heart disease (heart attacks) because that is the chief driver of the 20th-century cardiovascular disease pandemic. I have not addressed the enormous advances in treating congenital heart disease and the near elimination of rheumatic heart disease during this period. I have also not focused on heart failure, which is often the end stage of atherosclerotic coronary vascular disease but also has many non-atherosclerotic causes (especially hypertension). These deaths are generally tallied as “heart disease deaths” but not necessarily as “coronary heart disease” or “heart attack” deaths, and their trends are more difficult to parse. I have not discussed heart transplants, ventricular assist devices, and other treatments for end-stage heart failure. I have also not focused on stroke, for which we lack reliable data as to which are caused by atherosclerosis and which by bleeding (usually due to hypertension).
I have focused here on interventions that have been proven efficacious and have been sufficiently impactful to influence the course of the cardiovascular pandemic. I have recounted a few important “dry wells” that cardiovascular researchers have come across during their 50-year fight to curb the heart attack pandemic—specifically, cholesterol ester transfer protein inhibition (Chapter 8) and menopausal hormone therapy (Chapter 9). However, I have deliberately omitted many other less important blind alleys and dead ends in the interest of not bogging my readers down unnecessarily. For example, I have said little about the many clinical trials of the efficacy of the anti-oxidant vitamins C and E and beta-carotene in the prevention of heart attacks, none of which demonstrated any benefit. Many of these trials were factorial add-ons to trials of other more promising interventions like aspirin, ACE inhibition, and menopausal hormone therapy. I have also said little about omega-3 fatty acids (fish oils), since clinical trial evidence for their efficacy in preventing or treating heart disease is lacking.
Looking to the future, one can find cause for both optimism and concern. Our pharmacology and technology continue to advance rapidly. New avenues for intervention (e.g., anti-inflammatory drugs) hold promise. However, the U.S. is not doing well in the lifestyle arena, as evidenced by the rapidly rising tide of obesity and type 2 diabetes. Although we have been extraordinarily resourceful in finding drugs and medical procedures to compensate for our shortcomings in this area, it seems foolhardy to rely on drugs and technology to continue to bail us out from our continuing unhealthy lifestyle choices. Taking care to choose healthful foods and not to eat more calories than you can burn is tedious and less gratifying than placing a stent to restore blood flow in a blocked coronary artery or bringing someone back from the brink of death by a well-timed electrical shock. But the tedious course is more rewarding and sustainable. If we do not at least hold the line on diet and exercise and stem the rising tide of obesity and diabetes, cardiovascular mortality rates may begin to rise once again.