Patients with SAH were found to have myocardial necrosis. But instead of being centered around coronary arteries, it was found near intracardiac nerves!
The damage appeared neural, not ischemic, in origin.
9/ The question then becomes: how does bleeding into the subarachnoid space lead to sympathetic activation?
To answer this question, we need to examine adjacent structures that might be susceptible to injury after SAH.
10/ The hypothalamus is one structure adjacent to the subarachnoid space.
Given its role in the autonomic nervous system, one hypothesis suggests that hypothalamic irritation after SAH leads to sympathetic activation and cerebral T-waves.
11/ This is supported by animal studies from the 1960s showing that direct electrical stimulation of the hypothalamus leads to ECG changes (including TWI).
12/ Another structure that may be affected by SAH is the insular cortex, an area that lies buried in the sylvian fissure beneath the frontoparietal and temporal lobes.
🔑The insular cortex also plays a role in sympathetic regulation.
14/ Additional support for the sympathetic activation hypothesis comes from another condition associated with elevated catecholamines and deep/inverted T-waves:
15/ Cerebral T-waves in subarachnoid hemorrhage are just one example where sympathetic activation leads to deep TWI.
In the coming days, I'll add some other examples of what might be more accurately termed "sympathetic T-waves".
16/16
☞ Subarachnoid hemorrhage is associated with deep/inverted "cerebral T-waves"
☞ Cerebral T-waves are the result of sympathetic activation, either from injury to the hypothalamus and/or insular cortex
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You are seeing a patient recently diagnosed with heart failure and started on GDMT. You notice that their hemoglobin (HGB) has increased (12 → 13 g/dL) in the intervening weeks.
🤔Which medication is the likely cause of this increase in HGB?
2/12 - An Answer
Empagliflozin
💡All SGLT2 inhibitors have been associated with an increase in hematocrit/hemoglobin soon after initiation.
The average increase is 2.3% in hematocrit and 0.6 g/dL in hemoglobin.
The effect of SGLT2 inhibitors on HCT/HGB has been noted since the very first randomized control trial of dapagliflozin, published in 2010.
Initially, investigators assumed this was related to the diuretic effect of these drugs (i.e., a reduction in plasma volume led to an increase in HCT/HGB).
3/ The mutation in the Factor V gene conferring resistance to activated protein C was detailed the following year by a group in Leiden, The Netherlands.