September 1996 696 Shah et al. American Heart Journal
Fig. 2. Proximal stenosis of left anterior descending coronary artery (LAD) (left upperpaneD assessed by new system for quantitative analysis of three-dimensional intracoronary ultrasound images.~, 4 Cross-sec- tional ultrasound images were reconstructed in two perpendicular longitudinal sections (I and II, right up- per panels) and computerized contour detection was performed providing a three-dimensional view (left lowerpaneD and dimensions of lumen, plaque, and total vessel, calculated from area measurements. Mean diameter measurements (ram) of 200 consecutive ultrasound frames (right lowerpaneD are displayed, with plaque shown as white area between total vessel and lumen diameter. Note reduction of total vessel di- ameter from distal reference (mid-LAD) to target stenosis. Arrowheads in three-dimensional view and an- giogram indicate site of stenosis, which is also displayed in cross-sectional ultrasound view (mid-left upper panel). LM, Left main coronary artery; PROX, proximal.
mal translesional pressure-flow velocity measurements. J Am CoU Cardiol 1995;25:178-87.
7. Ge J, Erbel R, Zamorano J, Koch L, Kearney P, Gorge G, et al. Coro- nary artery remodeling in artherosclerotic disease: an intravascular ultrasonic study in vive. Coronary Artery Disease 1993;4:981-6.
Spontaneous coronary artery dissection in a young man with inferior wall myocardial infarction
Chetan Shah, MD, Dhiraj Narula, MD, Hema Kulkarni, MD, DM, and Bharat Dalvi, MD, DM Bombay, India
From the Department of Cardiology, King Edward VII Memorial Hospital.
Reprint requests: Bharat V. Dalvi, MD, DM, Department of Cardiology, King Edward VII Memorial Hospital, Parel, Bombay-400012, India.
Spontaneous coronary artery dissection is a rare cause of myocardial infarction. Its precise incidence, cause, patho- genesis, and treatment have not been clearly established. We report a young man who had an inferior wall myocar- dial infarction caused by spontaneous dissection of right coronary artery.
A 25-year-old man was referred to our unit for coronary angiography for his postinfarct angina. Patient had an in- ferior wall myocardial infarction 4 weeks earlier. He had no history of angina before infarction or risk factors for coronary artery disease. He had not had any chest trauma or viral infection preceding this infarction. He had no drug addiction or family history of premature coronary disease or sudden death. Patient had received nitrates, aspirin, atenolol, and heparin for 48 hours at the time of infarction. On clinical examination, his body habitus was normal and he had a blood pressure of 110/70 mm Hg. He did not have any stigmata of hyperlipidemia or collagen vascular dis- ease. The electrocardiogram was consistent with recent inferior wall myocardial infarction. Two-dimensional echo- cardiography revealed posterobasal and diaphragmatic hypokinesia and left ventricular ejection fraction of 45%.
Volume 132, Number 3 American Heart Journal Shah et al. 697
Fig. 1. Selective r ight coronary angiography in A, left anter ior oblique and B, in r ight anter ior oblique views showing l inear dissection in mid-r ight coronary a r te ry (arrowhead).
Rheumatoid ar thr i t i s factor was negative. The tests for an t inuclear ant ibodies and ant i -dsDNA were negative. His serum cholesterol level was 259 mg/dl, and serum triglyc- eride level was 140 mg/dl. His high-densi ty lipoprotein, low-density l ipoprotein, and very-low-density l ipoprotein cholesterol fractions were 45 mg/dl, 186 mg/dl, and 28 mg/ dl, respectively. His coronary angiography revealed a nor- mal left coronary ar te r ia l system. The r ight coronary a r te ry showed a long l inear dissection in the mid-r ight coronary a r te ry (Fig. 1A, B). Left ventr iculography showed posterobasal and d iaphragmat ic hypokinesia. He under- went an exercise tes t 6 weeks la te r t ha t revealed no evidence of reversible ischemia up to the fourth stage of Bruce's protocol a t a hea r t ra te of 195 beats /min (100% of max imum hea r t rate).
Coronary a r te ry dissection may occur from conditions such as aortic dissection, chest t rauma, prosthet ic valve replacement , and coronary a r t e ry bypass graft ing or after coronary angiography. 1 After coronary angioplasty, lim- i ted dissection is commonly seen, but i t forms a par t of the di la ta t ion process and can be called a "controlled injury." Very rare ly does coronary ar te r ia l dissection spontane- ously occur. The cause of such spontaneous dissection is uncertain. Three groups of these pat ients have been iden- tified: those associated with atherosclerotic coronary dis- ease, women in the pos tpa r tum period, and an idiopathic group without identif iable predisposing factors. 2 Since its first descript ion by Pret ty, 3 75% of the cases of spontane- ous coronary ar te ry dissection have been women and 25% have been men. 4 Dissection appears to be more common in the left coronary sys tem in women and in the r ight coro- nary a r t e ry in men, 5 as seen in our patient .
In most cases of spontaneous coronary dissection there is some evidence of atherosclerotic coronary a r te ry dis-
ease, 4 unl ike in our pa t ien t who had otherwise angiograph- ically normal coronary arteries. In t ravascu la r u l t rasound might conceivably detect plaques in pat ients with anglo- graphical ly normal arteries, but i ts use has not so far been described in the evaluat ion of spontaneous coronary dis- sections. In most of the repor ted cases, except in the post- pa r tum group, there was evidence of one or more r isk fac- tors for coronary a r te ry disease. 4 In the idiopathic group, to which our pa t ien t belongs, there are reports of eosino- philic inf i l t rates in the advent i t ia of the involved artery. 6 I t has been pos tu la ted tha t proteins or iginat ing from eosi- nophil ic granules may cause vessel wall damage with con- sequent dissection. Other autopsy series have demon- s t ra ted cystic spaces in the vessel media, which may have been the cause. 7
Thayer et a]. s recommended coronary a r te ry bypass graft ing for all pa t ients with spontaneous coronary dissec- tion. De Maio et al. 2 repor ted 82% survival on follow-up of 1.5 to 44 months (mean 38 months) and suggested tha t in- dications for surgical intervent ions in these pat ients should be the same as for those with fixed atherosclerotic disease. In tha t series, 3 of 25 (12%) survivers died at 48 to 132 months. However, recurrences have not been documented in this or other reports. 2, 4 I t remains to be seen whether the avai labi l i ty of s tents will influence the therapeut ic de- cisions. A good long-term prognosis is expected in our pa- t ient in l ight of l imited dissection and good luminal patency with no res idual ischemia demonst ra ted at high level of exercise. In conclusion, spontaneous coronary ar- tery dissection is ext remely rare and should be looked for in pat ients wi thout any r isk factors for coronary athero- sclerosis. Diagnosis can be made only at the t ime of coro- nary angiography. Indicat ions for surgery remain the same as with atherosclerotic coronary a r te ry disease. Im-
September 1996 6 9 8 Nigri et al. American Heart Journal
pact of newer nonsurgical techniques has not been evalu- a ted yet. Long-term prognosis is usual ly excellent in the absence of ongoing ischemia.
REFERENCES
1. Virmani R, Forman MB. Nonatherosclerotic myocardial infarction. In Virmani R, editor. Nonatheroscleretic ischaemic heart disease. Raven Press: New York, 1989, 325-54.
2. DeMaio SJ Jr, Kinsella SH, Silverman ME. Clinical course and long term prognosis of spontaneous coronary artery dissection. Am J Car- diol 1989;64:471-4.
3. Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42: rupture. Br Med J 1987;1:667.
5. Vackel JL, Phelix J, Dunn M. Spontaneous dissection of the left ante- rior descending artery in a male with survival. Cathet Cardiovasc Diag 1987;13:117-20.
6. Robinowitz M, Virmani R, McAllister H. Spontaneous coronary artery dissection and eosinophilic inflammation: a cause and effect relation- ship? Am J Med 1982;72:293-8.
7. Bulkley B, Roberts W: Dissecting aneurysm (hematema) limited to coronary artery: a clinicopathologic study of six patients. Am J Med 1973;55:747-56.
8. Thayer J, Healy R, Maggs P. Spontaneous coronary artery dissection. Ann Thorac Surg 1987;44:97-107.
Atrial natriuretic peptide release during myocardial ischemia induced by percutaneous transluminal coronary angioplasty
Antonio Nigri, MD, Gennaro Sardel la , MD, Carlo Tosti-Croce, MD, Eugenio Martuscel l i , MD, Francesco Pizzuto, MD, Cesare Greco, MD, and Andrea Berni, MD Rome, Italy
I t has been shown tha t acute myocardial ischemia induced by balloon inflat ion during percutaneous t r ans lumina l coronary angioplasty (PTCA) may increase the p lasma concentration of a t r ia l na t r iure t ic pept ide (ANP). Appar- ently i t is not the ischemia per se, but the ischemic left vent r icular failure tha t is the real cause of increased ANP production. 15 ANP is re leased main ly into the coronary si- nus; in fact, ANP concentration in the coronary sinus blood
in per iphera l blood. Thus is considerably higher than tha t 6 sampl ing blood from the coronary sinus should be a be t te r approach to evaluate var ia t ion in ANP production. We studied the effect of ischemia dur ing PTCA on ANP pro- duction by measur ing ANP p lasma concentration in the coronary sinus and a per iphera l vein.
Methods: The s tudy populat ion consisted of nine pa- t ients (8 men, I woman, aged 32 to 58, mean 49.4 years) undergoing elective PTCA for critical lesions of the left an- ter ior coronary ar te ry (8 pat ients) and the left circumflex coronary a r te ry (1 patient). Cathe ters were placed as fol- lows: (1) a 6F Cournand ca the ter in the coronary sinus from the left subclavian vein, (2) a Judkins type 8F guid- ing catheter into the left coronary ostium from the r ight femoral artery, and (3) a pigtai l ca the ter in the left v e n t r i - cle from the left femoral a r te ry (five patients) . An over- the-wire system was used for angioplasty. Blood samples for ANP p lasma level measurements were obtained from the coronary sinus and the r ight femoral vein at baseline, a t 60 to 80 seconds of balloon inflat ion during electrocar- diogram ischemic changes, and immedia te ly after balloon deflation. In five pa t ien ts left ventr icular pressure was si- mul taneous ly recorded. P l a sma ANP concentration was measured with a rad io immunoassay method (Nichols In- st i tute, Wij chen, The Nether lands) after isolat ion by means of affinity chromatography with a C-18 Sep-Pak cartr idge (Waters Associates, Milford, Mass.). I n t r aa s say var iabi l i ty was 6.7%, and in te rassay var iabi l i ty was 12%. The s tudy was designed to have the power of 0.80 to detect, wi th a significant level of 0.05, a difference in coronary sinus ANF concentrations before and dur ing ischemia of 450 pg/ml (SD 500). Sample size was es t imated to be n ine patients: Data , expressed as mean + SD, were analyzed by repea ted measures analysis of variance; s tudent ' s t tes t for pai red da ta was used to compare respective coronary sinus and per iphera l vein values.
Results: In all pa t ients PTCA was considered successful by the s t andard criteria; there were no complications. The ANP p lasma concentration of the coronary sinus blood was 382.6 _+ 532 pg/ml at basel ine and increased significantly to 700.6 _+ 679 during balloon inflation (p < 0.02); af ter balloon deflation the mean value was 301.7-+ 270, a significant fall from the peak ischemic concentration (p < 0.02). The per iphera l vein ANP p la sma concentrations were 27 +- 27 at baseline, 48 _+ 38 during balloon inflation, and 45.9 -+ 42 after deflation; the var ia t ions were not sta- t is t ical ly significant. All the per iphera l vein values were significantly lower in comparison with the respective cor- onary sinus concentrations (p < 0.05 for baseline, p < 0.01 for inflat ion and deflation values) (Fig. 1). The left ventric- u la r end-diastolic pressure increased during balloon infla- t ion from 16 +- 10 to 24.4 +-- 10, decreasing to 19.2 +-- 6 af- ter deflation; the var ia t ions were not s tat is t ical ly signifi- cant.
Comments: The increase in ANP production during my- ocardial ischemia induced by PTCA has been re la ted to is- chemic left ventr icular dysfunction with increased left ventr icular end-diastolic and left a t r ia l pressures. A corre- lat ion was found between pulmonary capi l lary wedge pressure 1, 3, 4 or r ight a t r ia l pressure 2 and ANP release during PTCA; this f inding is consistent wi th the s t re tching mechanism on a t r ia l myocites as the s t imulus to ANP re- lease. 7 In five of our pat ients we measured the left ventric- u lar end-diastolic pressure, which increased dur ing PTCA- induced ischemia but did not reach s tat is t ical significance,
