Early cholesterol-lowering drug therapy after hospitalization for acute coronary syndrome appears to reduce artery-clogging plaque, according to a new study. This was true even among patients who did not have very high low-density lipoprotein (LDL or ”bad”) cholesterol levels. Acute coronary syndrome includes unstable angina (chest pain), ST-elevation or non-ST elevation heart attack.
From American Heart Association:
Statin therapy for acute coronary syndrome may reduce plaque
Early cholesterol-lowering drug therapy after hospitalization for acute coronary syndrome appears to reduce artery-clogging plaque, according to a study reported in Circulation: Journal of the American Heart Association.
This was true even among patients who did not have very high low-density lipoprotein (LDL or ”bad”) cholesterol levels. Acute coronary syndrome includes unstable angina (chest pain), ST-elevation or non-ST elevation heart attack.
”This is the first evidence that plaque can regress with early statin treatment in heart attack patients,” said Shinya Okazaki, M.D., the study’s lead author and an instructor in the department of cardiology at Juntendo University School of Medicine in Tokyo. ”This evidence provides further support for the use of statins after a heart attack.”
Researchers studied 70 patients who had emergency procedures to re-open narrowed arteries after having heart attacks or unstable angina. Half of the patients received daily 20 mg doses of the cholesterol-lowering drug atorvastatin. The other half (control group) received a cholesterol-lowering diet. If their LDL cholesterol level was still very high (150 mg/dL or higher) a month later even with the diet, doctors prescribed a cholesterol absorption inhibitor.
”We hypothesized that the early statin treatment would reduce artery plaque volume after a heart attack and, therefore, would decrease one’s chance of having another heart attack,” Okazaki said.
Okazaki and colleagues measured each patient’s plaque volume using intracoronary ultrasound technology at the start of the study and after six months of therapy.
They found, at six months, that the LDL-C level was decreased by 41.7 percent in the atorvastatin group compared with a 0.7 percent increase in the control group.
The plaque in the vessel was reduced by an average of 13.1 percent in the atorvastatin group, but it increased — by an average of 8.7 percent — in the control group.
”The positive effect of atorvastatin was evident whether people went into the study with an LDL-C above 125 mg/dL or not, indicating that this lipid-lowering therapy would be beneficial whether people who have heart attacks have very high cholesterol or not,” Okazaki said. ”It could be that, when it’s given for six months immediately after heart attack, the therapy targets the ‘vulnerable,’ lipid-rich plaque in the vessel.”
Okazaki said early cholesterol-lowering may not only cause vulnerable plaque to regress, but might also stabilize it, although this was not assessed in this study. This could be an important way to reduce the chance of a recurrent heart attack — regardless of a patient’s LDL-C level. In this small, short-term study, there were no differences in cardiac events (heart attack, cardiac death, angina, repeat angioplasty or repeat bypass surgery.)
Future studies should examine how statin therapy stabilizes plaque early after a heart attack, as well as the effects of other new LDL cholesterol-lowering drugs, he said.
Co-authors are: Takayuki Yokoyama, M.D.; Katsumi Miyauchi, M.D.; Kazunori Shimada, M.D.; Takeshi Kurata, M.D.; Hitoshi Sato, M.D.; and Hiroyuki Daida, M.D.
