{'fraction_non_alphanumeric': 0.02027491408934708, 'fraction_numerical': 0.004123711340206186, 'mean_word_length': 5.287257019438445, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Can Statins Alter Coronary Plaque Morphology Assessed by Intravascular Ultrasound?

We read with interest the article by Hikita et al entitled ‘‘Impact of Statin Use Before the Onset of Acute Myocardial Infarction on Coronary Plaque Morphology of the Culprit Lesion.’’ They evaluated the impact of statin treatment before the onset of acute myocardial infarction (AMI) on coronary plaque morphology at culprit lesions by using intravascular ultrasound virtual histology (IVUS-VH) before percutaneous coronary intervention (PCI). They concluded that statin use before the onset of AMI might have effects on coronary plaque morphology of the AMI culprit lesion with less necrotic core and greater fibrous and fibrofatty component. Statin therapy, especially intensive doses, is associated with a decreased plaque size, lipid content, and thickness of the fibrous cap. Statins have pleiotropic effects that are independent of lipid-lowering effects. The pleiotropic effects of statins (anti-inflammatory and antithrombotic properties) are often greater with high doses of statins, and there may be individual differences among various statins. A study comparing 8 months of pitavastatin (4 mg daily) with pravastatin (20 mg daily) showed that pitavastatin induced a reduction in fibrous and fibrofatty tissue, but an increase in necrotic core while on pravastatin showed no effects on fibrous tissue and the necrotic core but a decrease in fibrofatty tissue. In the Hikita et al study, the statin doses are low and there is no information about the patients’ medication other than statins and whether there was statin loading before PCI. It would be useful if the authors provided information about the treatment duration of statins. Hikita et al evaluated the impact of statin treatment on coronary plaque morphology only at culprit lesions; it would be useful if they also evaluated nonculprit lesions. A 3-vessel gray-scale IVUS study showed that at least 1 plaque rupture was found somewhere other than at the culprit lesions in 79% of the patients with AMI. The results of the Providing Regional Observation to Study Predictors of Events in Coronary Tree (PROSPECT) trial provided data about the natural history of vulnerable plaques observed by gray-scale IVUS and IVUSVH. In this study, 697 patients with acute coronary syndrome underwent 3-vessel coronary angiography and IVUS study after PCI. At follow-up, recurrent clinical events were equally attributable to the culprit and nonculprit lesions. There have also been some concerns raised about the IVUS-VH because of its poor correlation with necrotic core in a porcine model. Although our goal must be the identification of vulnerable plaques before they rupture, assessment of ruptured plaques provides information regarding plaque vulnerability. Therefore, caution must be taken when drawing conclusions from studies using different IVUS approaches.