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Year : 2017  |  Volume : 6  |  Issue : 3  |  Page : 118-121

Medical angioplasty for iatrogenic malignant coronary atherosclerosis

1 Dr. Kunhali's Heart Care Center, Calicut, Kerala, India
2 Department of Internal Medicine, Baby Memorial Hospital, Calicut, Kerala, India

Date of Web Publication4-Jul-2017

Correspondence Address:
Robin George Manappallil
Baby Memorial Hospital, Calicut - 673 004, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2250-3528.209382

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The prevalence of coronary artery disease has drastically increased worldwide. The current guidelines recommend optimized medical therapy as the first-line treatment for stable angina; with revascularization reserved for those whose symptoms persist or progress despite intensive medical therapy. However, in the present world, many patients undergo revascularization as the first-line treatment, despite these recommendations. We report the case of a young obese female with stable angina, who underwent percutaneous coronary intervention for single vessel disease. Her symptoms aggravated post-procedure and was later found to have a lesion in the left main coronary artery (LMCA) causing 80% stenosis. In view of significant LMCA disease, she was advised revascularization but was not willing for the same. Hence, she was treated with optimal medical therapy and therapeutic lifestyle changes, which completely resolved her symptoms.

Keywords: Optimal medical therapy, percutaneous coronary intervention, stable angina

How to cite this article:
Kunhali K, Manappallil RG. Medical angioplasty for iatrogenic malignant coronary atherosclerosis. J Clin Prev Cardiol 2017;6:118-21

How to cite this URL:
Kunhali K, Manappallil RG. Medical angioplasty for iatrogenic malignant coronary atherosclerosis. J Clin Prev Cardiol [serial online] 2017 [cited 2023 Mar 29];6:118-21. Available from: https://www.jcpconline.org/text.asp?2017/6/3/118/209382

  Introduction Top

Atherosclerosis is a slowly progressive pathology taking several decades to reach a critical level. However, during the last couple of years, we have seen a number of patients developing rapidly progressive new lesions or rapid proliferation of preexisting minor lesions after angioplasty, stenting, and coronary artery bypass graft surgery. This can be justifiably termed as malignant atherosclerosis.

Optimal medical therapy (OMT) comprises intensive medical treatment, reduction of cardiovascular risk factors, and lifestyle modifications. Although the treatment guidelines recommend OMT as the initial approach to stable angina, countries like USA have witnessed a transition to percutaneous coronary intervention (PCI) as the initial management strategy over the past two to three decades.[1],[2] We report the case of a young obese female with stable angina whose coronary angiography (CAG) showed single vessel disease (SVD) and she underwent PCI. Two months later, she again developed progressive angina with worsening of symptoms in spite of medical treatment from her cardiologist. Her repeat CAG showed 80% lesions of left main coronary ostium. She was advised revascularization but refused the same, hence was started on OMT, following which her symptoms resolved completely within 10 days. She had further improvement in her effort tolerance at 6-months follow-up.

  Case Report Top

A 32-year-old, married female, homemaker, presented to us with a history of exertional angina (Canadian Cardiovascular Society [CCS] Class I) for the past 4 months. There was no history of coronary artery disease in her family. She had undergone CAG in another hospital which showed 80% stenosis at proximal left anterior descending (LAD) artery and 90% at first diagonal origin [Figure 1]; for which PCI with stenting was done. She was discharged on the following medications.
Figure 1: Coronary artery angiography showing left anterior descending stenosis

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Aspirin 150 mg once daily, clopidogrel 75 mg once daily, sustained-release metoprolol 50 mg once daily, glyceryl trinitrate 2.6 mg twice daily, and sublingual nitrate 5 mg (as needed).

About 2 months later, she again developed angina, but this time, it was progressive CCS Class III. She consulted another cardiologist (elsewhere) and a repeat CAG was done which showed patent proximal LAD stented segment with multiple areas of stenosis, i.e., 70%–80% at the ostium of left main coronary artery (LMCA), 30% at left circumflex ostium, and 30% at right coronary artery ostium [Figure 2]. She was advised PCI to LMCA but refused.
Figure 2: Coronary artery angiography showing multiple areas of stenosis

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On presentation to our hospital, she had CCS Class III angina. She was obese with weight of 68 kg, height 150 cm, and body mass index 30.22 kg/m 2. She had a heart rate of 74/min (regular) and blood pressure of 140/80 mmHg. Her systemic examinations were normal. Her blood investigations showed dyslipidemia (low-density lipoprotein cholesterol 191 mg/dL, high-density lipoprotein cholesterol 29 mg/dL, very low-density lipoprotein cholesterol 36 mg/dL, and serum triglycerides 265 mg/dL). Other investigations such as complete blood count, renal functions, serum electrolytes, liver functions, thyroid-stimulating hormone, and glycosylated hemoglobin were normal. Chest X-ray and echocardiogram were normal. Her electrocardiogram (ECG) showed nonspecific T-wave changes, and treadmill test (TMT) ECG was positive for inducible ischemia [Figure 3]. Since she was not willing for any percutaneous or surgical intervention, she was started on OMT which comprised therapeutic lifestyle change and medications as follows:
Figure 3: Treadmill test before optimal medical therapy

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Aspirin 150 mg once daily, clopidogrel 75 mg once daily, rosuvastatin 20 mg once daily, metoprolol 25 mg twice daily, amlodipine 2.5 mg twice daily, perindopril 2 mg once daily, nicorandil 5 mg twice daily, ranolazine 500 mg twice daily, trimetazidine 35 mg twice daily, glyceryl trinitrate 6.4 mg twice daily, and antioxidants.

After 10 days of therapy, she became completely asymptomatic. She had reduced her weight by 2 kg. Her heart rate was 64/min and blood pressure 110/70 mmHg. Her repeat TMT after 10 days did not show any ischemic changes even at ten metabolic equivalents of exercise [Figure 4]. She was discharged on OMT with regular follow-ups and continues to be symptom-free at 6 months follow up. Repeat TMT at 6 months showed further improvement in her effort tolerance. A comparative study of her TMT findings before and after OMT has been outlined in [Table 1].
Figure 4: Treadmill test after optimal medical therapy

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Table 1: A comparative study of exercise stress electrocardiogram findings

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  Discussion Top

The term angina pectoris was derived from the Greek word “ankhon” which means strangling and the Latin word “pectus” meaning chest. Stable angina refers to angina symptoms with no substantial changes over several weeks. These symptoms can fluctuate depending on myocardial oxygen consumption, temperature variations, and emotional stress.[3]

OMT aims at reducing the risk factors along with intensive medications. Risk factor modifications include weight reduction, exercise, yoga, control of heart rate, blood pressure, blood sugar, emotional stress, cessation of tobacco smoking, statin therapy, and dietary changes including low fat, low calorie, and high fiber with fresh fruits and vegetables. Factors that aggravate angina, i.e., hypertension, arrhythmias, left ventricular failure, strenuous activity, emotional stress and cold temperatures should be avoided. The necessary medications include platelet inhibitors and beta-blockers along with varying combination of nitroglycerin, long-acting nitrates, calcium channel blockers, ranolazine, nicorandil, trimetazidine, etc. The use of antioxidants is controversial.[3]

Several trials have compared the effectiveness of PCI and OMT in the management of stable angina. The Angioplasty Compared with Medicine (ACME) trial conducted on 200 patients comparing PCI with OMT in both single and multivessel CAD showed that patients with SVD had better symptomatic relief with PCI, but there was no difference in mortality or myocardial infarction, whereas those with multivessel CAD had no significant difference in terms of symptoms, mortality, or myocardial infarction. The Medicine, Angioplasty or Surgery Study (MASS) carried out on 200 patients with proximal LAD artery disease demonstrated no difference in the primary outcome (in terms of death, myocardial infarction, or refractory angina) in those subjected to OMT and PCI. The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial research group, which published the study on OMT with or without PCI for stable CAD, concluded that PCI did not reduce the risk of death or major adverse cardiovascular events in patients with severe CAD of one or more vessels on angiography or classic angina symptoms or documented ischemia on provocative tests, as compared to OMT. The Occluded Artery Trial which studied 2166 patients showed that there was more rapid symptomatic relief among the PCI group, but no statistically significant difference in long-term cardiac events as compared to OMT group.

The management approach to stable angina continues to be controversial. Factors such as cost, availability of technology, and expertise play a major role. Despite these controversies, OMT should be the initial treatment of choice in patients with normal/near normal left ventricular function with no or limited regional wall motion abnormalities, small perfusion defects and high threshold for angina. CAG should be planned only if symptoms persist after maximized OMT. In case of SVD not involving LMCA, OMT should be the first step. Revascularization should be reserved for those who are unable to tolerate OMT. In patients with multivessel disease and mild symptoms or normal systolic function, OMT can be an alternative treatment. Surgical revascularization would be the approach of choice in multivessel disease with impaired systolic function and in those with diabetes.[3]

  Conclusion Top

In this case, the patient was an obese female with symptoms of exertional angina. Her echocardiogram did not show any regional wall motion abnormality or left ventricular systolic dysfunction. OMT would have been a good treatment choice for her, particularly as her CAG showed SVD. However, she underwent percutaneous transluminal coronary angioplasty with stenting to LAD. Her angina symptoms worsened as she developed critical lesion of the LMCA within a couple of weeks; probably due to catheter injury of the intima inducing malignant atherosclerosis. The lesion could be a thrombus or atherosclerosis; but no thrombus was detected by CAG. At this point, though she deserved revascularization, she was treated with OMT alone because of her unwillingness to undergo any revascularization procedure. Remarkably, within a period of 10 days, she was rendered symptom free. This case thus once again demonstrates the value of OMT and emphasizes the need to consider OMT as the treatment of choice in patients with stable angina and, in a way to avoid iatrogenic complications.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina -- summary article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients with Chronic Stable Angina). J Am Coll Cardiol 2003;41:159-68.  Back to cited text no. 1
Smith SC Jr., Feldman TE, Hirshfeld JW Jr., Jacobs AK, Kern MJ, King SB 3rd, et al. ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention -- summary article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). Circulation 2006;113:156-75.  Back to cited text no. 2
Krishnaswamy A, Kapadia SR. Stable angina. In: Griffin BP, Topol EJ, editors. Manual of Cardiovascular Medicine. 3rd ed. New Delhi: Wolters Kluwer Pvt., Ltd.; 2010. p. 77-100.  Back to cited text no. 3


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1]


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