Page 43 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage
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Cardiac dysfunction after aneurysmal subarachnoid hemorrhage: relationship with outcome
Horizontal or down-sloping ST depression ≥ 0.05 mV in two contiguous leads; and/ or T inversion ≥ 0.1 mV in two contiguous leads with prominent R-wave or R/S ratio >1 were also considered ischemic changes. The Cornell voltage criteria (RaVL+SV3 > 28 mm(men) or > 20 mm(women)), or Sokolow-Lyon voltage index (SV1+RV5/6) >35 mm for left ventricular hypertrophy were used.
Echocardiography:
Transthoracic echocardiography was performed according to the standards of the
American Society of Echocardiography (ASE). Vingmed Medical Systems 7 were
used, one center used a Philips Sonos 7500 for 30 examinations. For assessment
of systolic function, three cardiologists (RB, MC, MG), independently from each 3 other and unaware of the clinical data of the patients, reviewed all echocardiograms
with the standard ASE 17-segment model for systolic function.9 All segments were scored based on contractility: 0 uninterpretable, 1 normal, 2 hypokinetic, 3 akinetic, 4 dyskinetic, 5 aneurysmal. A wall motion score index (WMSI) was calculated by dividing the sum of wall motion scores by the number of visualized segments. Diastolic function was assessed measuring pulsed wave Doppler of mitral valve peak velocity of early (E) and late (A) diastolic flow, early flow deceleration time, and duration of late flow. The E/A ratio was calculated from the mean E and A of three heart cycles. Pulmonary vein systolic (Ps) and diastolic (Pd) flow velocity, and atrial reversal flow duration (Adur) were also measured. Doppler tissue imaging (DTI) of the mitral annular motion was measured for early (E’) and late diastolic annular velocity and the ratio of the mitral E to the DTI E’ was calculated using the septal (E/E’) velocities. These parameters were then checked with the criteria on diastolic dysfunction according to the guidelines of the European Society of Cardiology.10
Laboratory results:
On admission, serum Troponin levels were determined, as a marker for myocardial damage. Additionally, N-terminal prohormone of B-Type Natriuretic Peptide (NT- proBNP) was measured which is a natriuretic hormone that, although first identified in the brain, is released from the heart in response to high filling pressures. Finally, Creatinine as indication of renal function was measured on admission. The upper limits of normal as defined by the local laboratory were used as reference.
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