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For at least 20 years, the Skeptical Cardiologist has been trying to communicate the current paradigm of coronary heart disease to his patients.
My job has been to translate the physician/scientific description of atherosclerosis: what happens to the arteries in the heart over time, how this results in heart attacks and angina, and what we can do to prevent symptoms, heart attacks, and death.
This description, written 8 years ago in a
Circulation editorial by Michael B. Rothberg, MD, of the Cleveland Clinic, is still a good scientific summary of the process of atherosclerosis: [W]e know that the interactions between dietary fat, serum cholesterol, and arterial endothelium are complex and dynamic. Although high-grade stenoses can cause chronic angina, most cardiac events occur at lesions that appeared mild on previous angiography. These plaques contain a lipid-rich core covered by a thin fibromatous cap. Inflammatory cells (eg, macrophages and mast cells) wi
JAMA Network Open highlights the lack of price competition in brand-name cardiovascular drugs that significantly impacts patient care.
It confirms what I ve noticed and been infuriated by when prescribing direct oral anticoagulants (DOACs) in clinical practice over the last 10 years.
When the first DOAC Boehringer Ingelheim s dabigatran (Pradaxa) was approved a decade ago, this oral direct thrombin inhibitor became the first new oral anticoagulant approved in the U.S. in more than 50 years. The RE-LY trial showed that 150 mg twice daily lowered the risk of stroke and systemic embolism by 35% beyond the reduction achieved with warfarin, which had been the standard of care for patients with non-valvular atrial fibrillation (afib).