While cocaine-induced myocardial in...

While cocaine-induced myocardial infarction has been repeatedly documented, the differential diagnosis of chest pain should include aortic pathology. The auspicious management of acute aortic dissection secondary to cocaine abuse has not been previously reported to our knowledge. In a 45-year-old man who not awayed with typical chest pain and wide mediastinum, the lucky management of this disease included early and accurate diagnosis and replacement of the aortic valve as well as the torn portion of the ascending aorta.

Clinicians are aware of the more commonly occurring cardiac and cerebrovascular events of cocaine abuse: ventricular arrhythmia, myocardial ischemia and infarction, cerebrovascular accident, and subarachnoid hemorrhage.[1-6] However, the differential diagnosis of chest pain associated with cocaine abuse should include aortic pathology. Acute break of the ascending aorta has been reported as a fatal deduction of smoking cocaine (freebasing).[1] This article is the first description, to our knowledge, of a felicitous antemortem diagnosis and repair of a cocaine-induced acute aortic dissection.

CASE REPORT

A healthy 45-year-old male executive, at the extremity of a 36-h drinking and cocaine-snorting session, existinged with severe, sudden, unrelenting, crushing substernal chest pain without radiation. There was associated upper back pain, along with diaphoresis and palpitations, unless without lightheadedness or leg, abdominal, or groin pain. The patient was initially evaluated at a nearby hospital and referr to North Shore University Hospital for definitive care.

Past medical history was significant for mild, untreated hypertension. The patient smok sum of two units packs of cigarettes and drank the same quart of vodka per day. He had had a fresh emergency room visit for mix with drugs overdose (IV heroin and cocaine--a speedball). There was no history of Marfan's syndrome or connective tissue disorder, nor were other medicines or other forms of cocaine used during this time.

Physical examination revealed moderate distress. His vital signs were as follows: heart rate, 100 bpm and regularly irregular; family pressure 148/60 mm Hg; and respiratory rate, 26 breaths/min. Cardiac examination showed a normal [Ssub1] and [Ssub2] with a decrescendo diastolic plaint at the left sternal border. There was no abrade or gallop. The left radial and left femoral pulsations were diminished, with no palpable oscillations distal to the left public femoral artery. The right radial and femoral measured [i]or[/i] regular beats were full and bounding. His urine output and laboratory values were within normal limits. The ECG showed sinus periodical emphasis with frequent atrial premature contractions, normal axis, and no evidence of acute infarction nor ischemia. A chest x-ray film showed clear lung fields with a widened mediastium.

Echocardiogram and CT scan recommended a Stanford type A acute aortic dissection. Angiography revealed a tear starting in the ascending aorta. The dissecting hematoma increaseed to the left common iliac artery (Fig 1) He was stabilized with IV propranolol and nitroprusside and transferred for surgical therapy.

At surgery the patient was placed forward cardiopulmonary bypass by femoral artery and right atrial cannulation. He was collecteded systemically to 25 [degrees] C and the heart was arrested with chill blood cardioplegia. A transverse tear was noted in the ascending aorta, which stretch outed around one-third of the aorta's circumference anteriorly. The dissection reach outed deeply into the noncoronary sinus of Valsalva, disrupting the aortic valve. The valve leaflets appeared thin and elongated. There was no annuloaortic ectasia, and the left ventricle was not enlarged. The aortic valve was replaced with a 27-mm Carpentier-Edwards porcine aortic prosthesis. The ascending aorta was completely excised from the horizontal just above the coronary ostia to just beyond the innominate artery. Teflon felt strips were placed inside and outside the aortic beats for reinforcement. The outside strips were soaked in salt-poor albumin and baked in an autoclave for 3 min to make them impermeable. A 30-mm low-porosity woven graft, which had also been soaked with salt-poor albumin and baked in an autoclave was then anastomosed to the couple aortic cuffs, proximal first and distal other After rewarming, the patient was remov from cardiopulmonary bypass, with estimable hemodynamic values and without ne for pressor or inotropic support.

The patient's postoperative course was complicated by way of an opportunistic pulmonary infection causing ventilatory prop requiring tracheostomy. His workup revealed him to be HIV positive. Discharge occurr forward the 47th postoperative day. At nine month postoperatively he has made a finished recovery with no disability.

DISCUSSION

Cocaine is a popular remedy used in many forms from one side all social strata. Acute aortic dissection must be considered in any patient with chest pain who admits to modern cocaine use. Previously reported causes of chest pain occurring during and immediately after cocaine use include myocardial ischemia or infarction,[2-4] myocarditis,[4] and pneumomediastinum.[7] Aortic disruption causing chest pain had not been previously reported, to our knowledge, in this clinical setting. It is impossible to determine the incidence of this potentially lethal complication, as many patients die before they prepare to a hospital, and a history of cocaine use may not be obtainable.[1,8] At presentation, the diagnosis may be missed or delayed if the focus is directed toward barely the cardiac rather than the vascular arrangements since cardiac complications have been the more commonly reported sequelae. Further delay in diagnosis can fall out as the patients may have no cardiovascular risk factors.[2-4,6] Although toxic flats of cocaine are frequently reported, there is a wide range of vital fluid concentrations measured among cocaine-related fatalities.[1,8] Therefore, a mix with drugs level is rarely useful.