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Spontaneous Regression of Subocclusive Coronary Stenosis: Does Time Heals All Wounds? | OMICS International
ISSN: 2155-9880
Journal of Clinical & Experimental Cardiology

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Spontaneous Regression of Subocclusive Coronary Stenosis: Does Time Heals All Wounds?

Salvatore De Rosa1, Annalisa Mongiardo1, Carmen Spaccarotella1, Daniele Torella1, Gianluca Caiazzo1 and Ciro Indolfi1,2*
1 Division of Cardiology, Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy
2 URT-CNR, Magna Graecia University, Catanzaro, Italy
Corresponding Author : Ciro Indolfi
Chief, Department of Medical and Surgical Sciences and Director
URT Consiglio Nazionale delle Ricerche (CNR)
Magna Graecia University, Catanzaro 88100, Italy
Tel: +3909613647151
Fax: +3909613647153
E-mail: [email protected]
Received January 22, 2014; Accepted March 29, 2014; Published April 05, 2014
Citation: De Rosa S, Mongiardo A, Spaccarotella C, Torella D, Caiazzo G, et al. (2014) Spontaneous Regression of Subocclusive Coronary Stenosis: Does Time Heals All Wounds? J Clin Exp Cardiolog 5:294. doi:10.4172/2155-9880.1000294
Copyright: © 2014 De Rosa S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Case Description
Surely the Beatles were not calling on interventional cardiologists in their last hit “Let it be”, even though it would have been a good advice in the present clinical case. We report, for the first time, on the spontaneous regression of a subocclusive coronary stenosis over 11 years.
A 52-years old man, with hypertension, dyslipidemia and previous NSTEMI, was referred to our hospital for coronary angiography, which revealed a subocclusive stenosis of the proximal 3rd obtuse marginal branch (OM3), with antegrade TIMI 0/1 flow and retrograde perfusion through the LAD (1A,1B) (Figure 1). The patient refused any intervention and was therefore discharged on secondary cardiovascular prevention, including antiplatelet therapy with ASA 100 mg/die and clopidogrel 75 mg/die, a statin (simvastatin 20 mg/die) and a betablocker (atenolol 25 mg/die). The patient underwent a cardiologic control every sixth month. Clopidogrel was stopped some months later, while atenolol dosing was repeatedly modified depending on Blood Pressure (BP) and Heart Rate (HR) levels. Similarly, ramipril 5 mg/die and nitrates were prescribed for some time and stopped again during the follow up.
Eleven years later, the same patient was referred again to our hospital with the diagnosis of STEMI of the anterior wall after successful thrombolysis. Pharmacological treatment at presentation included ASA 100 mg/die, clopidogrel 75 mg/die, atorvastatin 80 mg/die, ramipril 5 mg bid, furosemide 25 mg/die, atenolol 50 mg/die. Coronary angiography revealed residual critical stenosis of the proximal LAD with thrombotic stratification which was successfully treated with stent-PCI. Very interestingly, the previously subocclusive OM3 stenosis was spontaneously regressed to a 70% stenosis with a TIMI III flow (1C,1D) (Figure 1). The patient was then discharged on the following therapy: ASA 100 mg/die, ticagrelor 90 mg b.i.d., atorvastatin 80 mg/ die, ramipril 5 mg/die, furosemide 25 mg/die, atenolol 50 mg/die, spironolactone 25 mg/die. Importantly, the initial lesion was surely not a catheter-induced spasm, giving the distal position, nor any coronary wire had been inserted into the vessel. Furthermore, both angiograms were obtained after intracoronary nitroglycerin administration.
Thus the question remains: what was responsible for lesion regression in this patient? It is known that aggressive cholesterol lowering with statins slows progression of atherosclerosis, reduces new lesions’ formation or even causes atheroma regression and prevents clinical events [1,2]. On the other hand the beneficial effects of increased HDL-C are also recognized [3].
Our patient had stable LDL-C levels. However HDL-C levels were substantially increased from the initial evaluation in 2002 throughout the follow up. In addition, a much better Blood Pressure (BP) control was achieved. Since the patient had significantly increased his physical activity after the initial evaluation in 2002, it is tempting to speculate this contributed to the observed improvement in HDL-C levels and BP control. Altogether, the increase in HDL-C levels, the improved BP control and the regular exercise could have contributed to the regression of the coronary stenosis.
In conclusion, the present report is the first one showing spontaneous regression of a subocclusive coronary artery stenosis. However, no conclusion can be reached on the underlying mechanisms.
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