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Invited Commentary
August 2016

Slowing Progress in Cardiovascular Mortality Rates: You Reap What You Sow

Author Affiliations
  • 1Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
  • 2Division of Cardiology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
JAMA Cardiol. 2016;1(5):599-600. doi:10.1001/jamacardio.2016.1348

There are few public health success stories greater than the dramatic declines in cardiovascular disease (CVD) mortality rates achieved from about 1970 to 2010 in almost all Western countries. In many countries, age-adjusted death rates fell 70% or more during this period. Driven by the critical observations of epidemiologic studies and by novel insights into cardiovascular disease pathogenesis, there were major leaps forward in our ability to prevent CVD events and prevent fatality among those with acute CVD events such as myocardial infarction, stroke, and acute decompensated heart failure.

The recognition of causal risk factors, including tobacco use, atherogenic cholesterol profiles, elevated blood pressure, and dysglycemia and their upstream enablers of unhealthy dietary patterns and sedentary lifestyle, led to widespread public health initiatives, societal/environmental changes, and individual behavioral changes. In turn, these facilitated substantial reductions in smoking prevalence, lower cholesterol levels, and somewhat lower blood pressure levels in the US population (primordial and primary prevention). At the same time, the introduction of evidence-based preventive medications targeting blood pressure and low-density lipoprotein cholesterol reduction to treat individuals at risk for CVD (primary prevention) has increasingly reduced incident CVD events. Just as important in reducing CVD mortality rates was the sequential introduction of evidence-based therapies for individuals with acute CVD events and improved care after these events (secondary and tertiary prevention). Training of hospital staff in resuscitation and defibrillation; use of aspirin, β-blockers, antithrombotics, angiotensin-converting enzyme inhibitors, and statins; use of thrombolytics and primary revascularization strategies for acute myocardial infarction and stroke; and improved surgical and catheter-based revascularization techniques and heart failure care all appear to have contributed to reductions in CVD mortality over the decades. Thus, both public health and health care progress contributed roughly equally to these declines.1 Indeed, the inflection point in CVD mortality rates in the United States, when increases observed for the entire 20th century suddenly flipped to sustained declines, occurred in 1968, shortly after the US Surgeon General’s first report on tobacco and coincident with the introduction of coronary care units for patients with acute myocardial infarction.