Accelerated Atherosclerosis: How Fast Can It Develop?

Atherosclerosis is a chronic inflammatory reaction of the arterial wall. The etiopathogenesis of atherosclerosis is multifactorial and includes inflammatory, infectious, metabolic and immune system involvement. Accelerated atherosclerosis is the malignant form of disease, and is typically reported with vasculitis/collagen vascular disease.¹ We report a patient with accelerated atherosclerosis who had severe atherosclerotic progression of coronary artery disease over the 5-month period that followed his myocardial infarction (MI), despite being adequately treated for various risk factors. We propose that post-MI psychological stress as a possible explanation for such severe progression of the disease. Case Report. A 54-year-old male chronic smoker, who was normotensive and asymptomatic, had an acute inferior wall MI in May 2005. He was thrombolyzed with streptokinase. He was also diagnosed with diabetes mellitus during the same admission. The patient underwent coronary angiography in June 2005 because of recurrent episodes of angina. It revealed 90% type B lesion in the distal right coronary artery (RCA) (Figure 1A), an eccentric plaque followed by a 70% type A lesion in distal left circumflex artery (LCx) (Figure 1B), and a normal left anterior descending artery (LAD) (Figures 1B and C). In the same procedure, a 3 x 28 mm Bx Sonic™ stent (Cordis Corp., Miami, Florida) was deployed in the distal RCA, with favorable results (Figure 1D). From September 2005 onward, i.e., 3 months after percutaneous coronary intervention (PCI), the patient again began experiencing exertional and rest angina. A repeat angiography in November 2005, 5 months after PCI, revealed significant diffuse disease of the proximal to distal RCA (Figure 2A), the distal LCx (Figure 2B), the mid and distal LAD and diagonal (D2) arteries (Figures 2B and C). Left ventriculography revealed no regional wall motion abnormality, no mitral regurgitation and an ejection fraction of 60%. He had on-pump bypass surgery, receiving a left internal mammary graft to the diagonal (D2), a saphenous venous graft to the posterior descending artery of the RCA and the obtuse marginal of the LCx. The diffusely-diseased LAD was nongraftable. He had an uneventful postoperative recovery. The patient’s serum lipid profile in November 2005 on atorvastatin 20 mg/day was a total cholesterol of 109 mg%, an HDL of 25 mg%, and an LDL of 63 mg%, and his triglycerides were 103 mg%. His serum homocysteine was 20.7 µmol/liter and his lipoprotein(a) was 9.9 mg/dl. The patient’s diabetes was well controlled with oral hypoglycemic agents over the previous 5-month period; his HbA1C was 6%. The patient’s collagen profile-like rheumatoid factor, antinuclear antibody, antineutrophilic cytoplasmic antibody and anticardiolipin antibodies were negative. He is doing well on follow up 5 months after his bypass surgery. Discussion. Post-PCI accelerated atherosclerosis of an intervened vessel can be clearly explained by balloon catheter or stent-induced injury. However, the patient featured here had accelerated atherosclerosis of all three vessels, despite control of risk factors such as smoking cessation, blood sugar and dyslipidemia, and control of such normal nonconventional risk factors as lipoprotein(a) and homocysteine. His negative collagen workup ruled out the possibility of vasculitis or collagen vascular disease, which is one of the causes of accelerated atherosclerosis.¹ The only possible explanation of such severe accelerated atherosclerosis over a 5-month period is post-MI psychological stress.² The psychological stress causes platelet and neuroendocrine activation, which results in endothelial injury and dysfunction.² In the setting of insignificant atherosclerotic coronary artery disease, the endothelial injury and platelet activation can result in accelerated atherosclerosis in over the course of time, as happened in this case. Long-standing diabetes with associated macro- and microvascular complications and uncontrolled hyperglycemia is another cause for accelerated atherosclerosis,³ however, since our patient’s diabetes was recently diagnosed (May 2005), with no complications such as nephropathy, neuropathy or retinopathy, and since his sugar was well controlled with drugs (HbA1C 6%), it is unlikely that diabetes contributed to the accelerated atherosclerosis that occurred over the 5 months following his angioplasty procedure. Another practical point to bear in mind during the management of such cases is the poor outcome of revascularization. The follow-up angiogram was performed to look for possible in-stent restenosis in the RCA. However, it revealed severe, new-onset atherosclerotic disease of all 3 vessels. In such cases, it is difficult to determine the extent of multivessel revascularization that should be performed at a given point. In conclusion, interventionalists rarely encounter patients in their routine clinical practice who have such severe accelerated atherosclerosis.

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