Cardiac complications after SAH may cause sudden death [14, 25]. There are studies in the literature adressing the cardiac problems seen after SAH. The authors mostly identified increased sympathetic activity.
In dogs, experimental studies revealed high plasma catecholamine levels [4, 5, 9], myocardial necrosis , micro infarctions with electron microscopy , left ventricular dysfunction [5, 11] and wall motion abnormalities .
In clinical studies, in SAH patients, chances of ECG, high cardiac markers [1, 7, 15, 25], wall motion abnormalities [7, 25] were noted. Szabo et al. investigated myocardial perfusion with myocardial scintigraphy. They reported that myocardial ischemia might be seen without specific ECG changes .
In their post mortem examinations, Doshi & Neil-Dwyer found necrosis of individual muscle fibers, increased eosinophilia and granular cytoplasm, necrotic muscle fibers surrounded by macrophages . Sugiuro et al., in a case report (50 year old women), noted ECG changes indicating myocardial damage, high cardiac enzymes, hypokinetic left vetricular septum, pulmonary edema. Autopsy of the patient revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without the evidence of coronary artery occlusion . Yuki et al. in their case report reported ECG findings resembling myocardial infarction in a patient. Left ventriculography revealed cardiac dysfunction. Two months later, in the postmortem examination of the patient, after her death from cancer, no evidence of myocardial necrosis was revealed . The authors discussed coronary vasospasm and reversible postischemic stunned myocardium without necrosis which might happened after SAH .
In ischemic cardiac events, since intracellular enzymes and proteins increase in serum after the occurence of tissue necrosis , they may be insufficient in the diagnosis in the lack of necrosis or in cases where necrosis did not happen yet. Sinha et al., examined IMA, ECG and cTnT in patients who were admitted to an emergency department with acute chest pain. The sensitivity (82%), specifity (46%), negative predictive value (59%), positive predictive value (72%) of IMA were calculated. On contrary the sensitivity of ECG (45%) and cTnT (20%) were noted. They underlined the possible role of IMA in detecting ischemia before necrosis happen . In our experimental SAH study, in rats, we could not demonstrate significant changes in CK, AST and LDH tests when compared with control group at days 1, 2 and 7. There were significant increases of IMA at 7th day after SAH compared with the control group. We observed that the serum albumin values for all groups did not differ from the control group, thus we can say that high IMA in SAH may not be due to low albumin levels.
In the light microscopic examination myocardial necrosis was not seen in all groups but total injury scores of heart and lung tissues at days 1, 2 and 7 were found increased when compared to the control group. Also in days 1, 2 and 7 myocytolysis, which was described by Turillazzi as a specific histological marker of congestive heart failure without relation to coronary blood flow, myocardial hypoxia and myocardial fibrosis , was found increased compared to the control group. Both total injury scores of heart and lung tissues and myocytolysis of heart tissue at days 7 were found significantly increased compared to days 1 and 2.
In literature research we did not find an experimental study investigating IMA after experimental SAH.
There were clinical studies in the literature referring to increases of IMA after myocardial ischemia , transient myocardial ischemia , acute coronary syndrome [22, 28].
There were studies investigating IMA changes after pulmonary emboli , skeletal muscle ischemia [31–33] and cerebrovascular events including SAH [23, 34].
Zapica-Muniz et al., after skeletal muscle forearm ischemia test, in their volunteer subjects, found decreased levels of IMA at 1st, 3rd and 5th minutes compared to baseline values, in addition to low ammonia and high lactate levels. In lactate serum pool the authors found decreased levels of IMA after increases in lactic acid concentrations. The authors underlined the decreased diagnostic sensitivity of IMA because of increased lactate levels .
Roy et al., in their patients with peripheral vascular disease (PVD) and leg claudication, performed an exercise test inducing leg ischemia and found decreased levels of IMA during stress peak. They also performed a dobutamin stress echocardiography and found unchanged levels of IMA. In their patients regional wall motion abnormalities were not detected. They noted ischemia of tissues other than myocardium might be responsible for decreases of IMA .
IMA levels were found increased in volunteers of a marathon race for 24–48 hours . In another study Falkensammer et al. noted increased IMA levels after calf muscle ischemia induced by exercise in volunteers .
Sbarouni et al., in their review article, stated that the changes of IMA after exercises were not homogenous, they might be due to ischemic areas in the gastrointestinal tract and skeletal muscle. They also underlined that the role of hemoconcentration seen after physical exercises, might cause increases of albumin serum levels and because of decreased unbound cobalt to albumin, IMA might be lowered. They noted interference of lactic acidosis with IMA analysis .
Han et al. demonstrated increases in IMA after cerebral infarction, intracerebral hemorrhage and SAH (18 patients) compared to control group and they stated a positive correlation between IMA and lipid levels. In this study, patients with pulmonary emboli and coronary artery thrombosis within 6 months were excluded .
Gündüz et al. examined and compared the levels of IMA in intracerebral hemorrhage, SAH and brain infarction patients within 24 hours after their symptoms started. They found increased levels of IMA compared to control patients, and in brain infarction the increases were significant compared to SAH, and they stated that this finding might be used in differential diagnosis of SAH with brain infarction. The authors excluded patients with acute coronary syndrome, acute myocardial infarction, cardiac insufficiency, and pulmonary embolism in their study .