the complications related to drug abuse such as myocardial insufficiency , myocardial infarction , endocarditis , myocarditis , aortic dissection , neurologic damage , ischemic colitis and renal failure are known , but have been reported very rarely . amongst the illicit drugs , cocaine , amphetamines and cannabis have been studied and documented well to cause myocardial infarction by different mechanisms .
there is very sparse data available on myocardial involvement after heroin abuse.[13 ] here , we report a young male who suffered from acute myocardial injury after heroin inhalation .
a 28-year - old young male shopkeeper was brought to the emergency with complaints of chest discomfort , cold sweating and severe generalized weakness .
there was no history of fever , headache , any flu - like symptoms , systemic illness or drug allergy .
his parents were alive and there was no history of diabetes mellitus , coronary artery disease , hypertension or cerebrovascular disease in first degree relatives .
he was not a cigarette smoker but his parents and patient himself gave history of heroin inhalation ( smack ) for last five years .
as per history last heroin inhalation was done approximately 12 h before admission along with alcohol binge drinking . on general physical examination he was thin built , looked drowsy but arousable .
his vital signs were pulse 64/min , blood pressure 70/50 mmhg , respiratory rate 24/min and temperature was 98.6f along with cold extremities .
laboratory data showed mild leukocytosis with total leukocyte count of 14,200/ cmm , hemoglobin 14.6 gm% , platelet count 2.6 lacs / cmm .
biochemical investigations including urea , creatinine , total protein , albumin , liver transaminases , glucose and fasting lipid profile were within normal limits .
value<20u / l ) total cpk was 456 u / l(normal being < 200 ) and toponin - i was 3.02 ng / ml ( normal value < 0.01 ng / ml ) . in 2-d echocardiography hypo kinesis of
left ventricular anterior wall was noticed while left ventricular systolic function and ejection fraction was within normal limits ( 64%).on the basis of history , clinical examination and investigations , diagnosis of acute coronary ischemic event involving left ventricular wall was made .
since the patient had hypotension at presentation , he was treated with aspirin 325 mg and clopidogrel 300 mg and vasopressors , but nitroglycerine could not be given to him .
the patient did not receive thrombolytic therapy , because of the pattern of electrocardiographic changes and time interval between the onset of chest tightness and hospitalization was more than 12 h. therefore , he was administered only subcutaneous low molecular weight heparin enoxaparin .
he responded to treatment , got relief in the chest discomfort and was discharged after seven days . at the time of discharge , minimal st elevation persisted in electrocardiogram which became normal after a week during follow up along with the echocardiography .
coronary angiography which was done one month later did not reveal any significant luminal stenosis .
the patient was diagnosed to have acute myocardial involvement on the basis of symptoms of chest tightness , cold sweating and hypotension .
his investigations that included electrocardiogram , echocardiography , cpk - mb and troponin - i and also favored the diagnosis of acute myocardial injury .
he had bilateral constricted pupils with excessive salivation , basal crepitations in the chest and relative bradycardia despite hypotension .
there was a definite history of heroin inhalation and binge drinking in the night prior to admission .
no family history of premature heart disease or any conventional risk factors of cardiovascular disease were present in the patient .
our patient presented with symptom of chest tightness , which was not localized , had no postural variation or relation with respiration .
he possibly had acute myocardial ischemia which is being supported by elevated cardiac biomarkers , electrocardiographic changes and echocardiography .
myocarditis can also masquerade as myocardial ischemia sometimes because of st - t changes , cardiac enzyme elevation and wall motion abnormalities which can be observed with myocarditis .
myocarditis was a possibility in our patient that could not be excluded . during the hospitalization we could not subject the patient for either coronary angiography or myocardial scintigraphy to confirm the infarct or any occlusive lesion in the coronaries .
heroin ( diacetylmorphine ) is rapidly hydrolyzed to 6-monoacetylmorphine which in turn is hydrolyzed to morphine . though heroin - induced myocardial infarction has been seldom reported , the underlying mechanisms have been still unclear .
reported a case of heroin intoxication followed by rhabdomyolysis associated with myocardial injury , with symptoms , laboratory findings , ecg and echocardiography features of non - q wave infarction .
however , a 201 thalium myocardial scintigraphy , performed after patient was discharged , did not show any abnormality .
this shows that heroin probably has a direct myotoxic effect on both myocardium and skeletal muscle .
there is a possibility that hypoxia , acidosis , vasoconstrictive substances released by muscle necrosis , or hypersensitivity reactions associated with heroin or some of its adulterants are involved in myocardial injury .
reported a young woman with acute myocardial infarction after heroin abuse ; they had claimed that heroin might have a direct toxic effect on the coronary arteries and can cause coronary occlusion by provoking vasospasm or inflammation .
there has been suggestion that heroin acts directly on vasomotor centre to increase parasympathetic activity and reduces sympathetic tone , which leads to vasodilatation and stimulates histamine release from mast cells .
. there was history of binge drinking present in our patient which has been associated with development of acute myocardial infarction .
men who consume five drinks ( 50 g ) or more and women who consume four drinks ( 40 g ) or more in single sitting are known as binge drinkers .
it is well known that ethanol induces concentration dependent vasospasm in coronary arteries and coronary vasoconstriction may itself damage the endothelium thereby increasing the likelihood of platelet adhesion and thrombus formation . in conclusion , a 28-year - old young male developed acute myocardial injury after heroin inhalation and binge drinking while he had no other conventional cardiovascular risk factors .
the cause might be heroin - induced cardio toxic effect or vasospasm compounded by the presence of binge drinking .
 amongst the illicit drugs cocaine , amphetamines and cannabis have been studied and documented well to cause myocardial infarction by different mechanisms but there is very sparse data available on myocardial involvement after heroin abuse . 
 we report a young man who developed acute myocardial injury after heroin inhalation and alcohol binge drinking . 
 heroin induced cardio toxic effect and vasospasm compounded by alcohol were suspected to be the cause of this . 
INTRODUCTION
CASE REPORT
DISCUSSION