Calcific embolization from aortic stenosis may be more resort to frequently than commonly appreciated.

Calcific embolization from aortic stenosis may be more resort to frequently than commonly appreciated. principally calcific emboli are clinically silent, although transient ischemic attacks, cerebral infarcts, blindness (from central retinal artery occlusions), and myocardial infarctions have been reported. We describe a patient with calcific bicuspid aortic stenosis who quick in emergenciesed with transient ischemic attacks and angina secondary to a calcific embolus to the inferior circumflex marginal coronary artery. The calcific embolus was retrieved during aortic valve replacement surgery A review of the literature insinuates that calcific embolization from calcific aortic stenosis may come to one's mind more commonly in patients with bicuspid valves.

While calcific aortic stenosis can issue in multiple hemodynamic alterations and cardiac symptoms, it can sometimes ready with symptoms related to vascular insufficiency becoming to calcific embolization.[1-5] These symptoms may provide the indication for surgical replacement of the valve equable in the absence of strict valvular stenosis or symptoms of swoon congestive heart failure, or angina.[1-3] We describe a patient with strict calcific bicuspid aortic stenosis, exertional angina, and transient ischemic attacks (TIAs), who had documented calcific embolization to a coronary artery.

CASE REPORT

A 45-year-old man with a history of a heart grumble since childhood presented to the Neurology Service with complaints of left-sided weakness and imbalance. The symptoms completely resolv by means of the time of presentation. Neurologic workup, including comput tomographic (CT) scan and magnetic resonance imaging (MRI) of the head as well as carotid duplex studies, was essentially normal. The patient denied any symptoms of congestive heart failure or frank elision He had a history of coarctation repair at the age of 19 years and in the past small in number years had experienced dull substernal chest pain radiating to the throat and associated with exertion. Physical examination was remarkable for delayed carotid pulsation decreased [A.sub.2] and a late peaking grade 4/6 systolic ejection whimper at the base. A grade 2 to 3/6 diastolic beat at the left sternal border was also noted. The ECG revealed normal sinus rhyme with a left anterior hemiblock and T-wave inversions in [Vsub4] to [Vsub6]

An echocardiogram revealed a calcified bicuspid aortic valve with decreased excursion, moderate aortic insufficiency, and a dilated aortic parent An aortic valve gradient of 42 mm and an aortic valve area of 07 [cmsub2] were obtained.

At cardiac catheterization, normal right-sided compressings were noted. Attempts to cros a extremely calcified aortic valve with multiple catheters failed. Coronary arteriography revealed a calcific filling deficiency at the bifurcation of a large inferior obtuse marginal branch of the left circumflex artery that riseed in an approximate 70 percent stenosis (Fig 1) No other coronary artery disease was noted. A 3+ aortic insufficiency and a dilated and aneurysmal ascending aorta were seen during aortic radical injection.

In light of the clinical and echocardiographic evidence of accurate aortic stenosis associated with symptoms of angina and transient ischemic attacks, as well as evidence of calcific embolization from the aortic valve, the patient underwent aortic valve replacement with a 25-mm aortic homograft. The ascending aorta was also replaced with a 38-mm Dacron interposition graft. The removal of the large calcific embolus, adherent to the intima of the secondary obtuse marginal artery, required a localized endarterectomy. The canal was patched with a saphenous vein bypass graft from the aorta. The patient tolerated surgery without complications. He is symptom liberated 20 months after surgery. Examination of the aortic valve revealed a raw area onward the ventricular surface of the valve that, chiefly likely, was the site for calcium breakage and embolization (Fig 2)

DISCUSSION

The first report of calcific embolization from calcific aortic stenosis was described at Moragues and associates[6] in 1950 Holly and coworkers[7] from the Mayo Clinic reported their observations of spontaneous calcific embolization in 31 of 165 autopsy cases with calcific aortic stenosis. Of these, 10 patients (6 percent of the total) had major coronary emboli (with a size of 1 to 3 mm) Soulie and associates[8] reported 28 cases of spontaneous calcific emboli in 81 patients with calcific aortic stenosis. This incidence was twice that observ with calcific mitral disease. The common occurrence of macroscopic coronary embolization caped 20 percent in the whole series (18 of 81 patients).

throughout the past two decades, scarcely any reports have been published describing patients who sustained clinical sequelae of spontaneous calcific embolization from calcific aortic stenosis. Patients were described with clinical evidence of cerebral emboli resulting in strokes[1] or TIAs[3,4] and emboli to the central retinal artery,[2] yet no other explanation for these symptoms. single in kind report[5] described a patient with calcific aortic stenosis who neared with an inferolateral myocardial infarction and obstruction of a distal branch of the left circumflex artery that was suspected still not proven to be secondary to embolization from the aortic valve. Angina in a patient with calcific aortic stenosis is more commonly related to the vicinity of atherosclerotic coronary artery disease. However, calcific embolization should be considered as the likely cause if the patient currents with sudden onset of chest pain. Our patient had stable angina and TIAs and was proven to have spontaneous coronary embolization resulting in narrowing of the marginal coronary artery noted onward angiography. Other reports in the literature describe calcium emboli from stenotic aortic valves associated with cardiac catheterization[9-11] or percutaneous balloon valvuloplasty[12,13] resulting in cerebral infarctions,[9,12] myocardial infarctions,[11-13] or leg ischemia.[10] In the latter case, the embolus was surgically retrieved from the left femoral artery.

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