Tony Breu Profile picture
Aug 7, 2022 16 tweets 7 min read Read on X
1/16
🤔Why does subarachnoid hemorrhage lead to deep/inverted "cerebral T-waves"?

This ECG finding is so dramatic. But as we will see, these patients often have normal hearts.

Why does an issue in the brain manifest on a test of the heart?
2/
Cerebral T-waves have been observed for decades.

🔑Though they have been seen in multiple forms of stroke, subarachnoid hemorrhage (SAH) is most closely linked with their appearance.

pubmed.ncbi.nlm.nih.gov/13313536/
3/
In 1960, Cropp reported a case of T-wave inversions (TWI) secondary to SAH. Surgery was delayed for fear of myocardial infarction (MI).

An autopsy showed no evidence of MI or chronic coronary artery disease.

💡Something else was causing the TWI.

pubmed.ncbi.nlm.nih.gov/13812988/
4/
Many theories have been proposed to explain cerebral T-waves.

🔑An increase in sympathetic tone, either systemically or localized to the heart, are part of most theories.

pubmed.ncbi.nlm.nih.gov/12138415/
5/
A 1991 study found that in patients with subarachnoid hemorrhage, high norepinephrine levels were associated with inverted T-waves.

pubmed.ncbi.nlm.nih.gov/2057973/
6/
But not all studies agree. Others have found that plasma norepinephrine concentrations do not parallel electrocardiographic abnormalities.

💡Maybe the sympathetic activity is local, not systemic.

pubmed.ncbi.nlm.nih.gov/8891057/
7/
This possibility was suggested in 1969.

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.

pubmed.ncbi.nlm.nih.gov/5782382/
8/
The results of the study in tweet 7 were felt to be mediated by the LOCAL release of norepinephrine from nerve endings.

🔑Whether systemic or local, sympathetic activation appears to be part of the genesis of cerebral T-waves.

pubmed.ncbi.nlm.nih.gov/5782382/
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.

pubmed.ncbi.nlm.nih.gov/7359184/
11/
This is supported by animal studies from the 1960s showing that direct electrical stimulation of the hypothalamus leads to ECG changes (including TWI).

pubmed.ncbi.nlm.nih.gov/13843556/
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.

ncbi.nlm.nih.gov/pmc/articles/P…
13/
Just as with the hypothalamus, the insular cortex is susceptible to injury after SAH.

💡It may be that damage to the insular cortex leads to sympathetic activation resulting in cerebral T-waves.

pubmed.ncbi.nlm.nih.gov/19813104/
14/
Additional support for the sympathetic activation hypothesis comes from another condition associated with elevated catecholamines and deep/inverted T-waves:

⚡️Takotsubo (stress) cardiomyopathy⚡️

The TWIs are often identical in appearance.

pubmed.ncbi.nlm.nih.gov/25981361/
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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More from @tony_breu

Nov 16, 2024
1/14
🤔 Why do we use iodine as an intravenous contrast agent?

The answer requires a review of the composition of the human body and a brief tour of one of my favorites, the Periodic Table of Elements. Image
2/
To begin, it's essential to understand which elements make up the human body. Amazingly, just six compose >98% of your weight:

➤Oxygen: 61% (varies based on water composition)
➤Carbon: 23%
➤Hydrogen 10%
➤Nitrogen: 2.6%
➤Calcium: 1.0%
➤Phosphorus: 0.6%

buff.ly/3YU4dIYImage
3/
One thing you'll notice about these six elements is that they are relatively small (i.e., they have low atomic numbers, aka are low-Z elements).

In addition to being the most prevalent elements in the universe, their low atomic number allows them to more readily form stable chemical bonds.Image
Read 14 tweets
Jun 22, 2024
1/7 - The Mystery

A patient presents with fever and confusion. After multiple weeks without a diagnosis, an astute clinician suggests a random skin biopsy.

The patient has no rash or dermatologic symptoms. And yet, the biopsy reveals the diagnosis.

🤔What is the condition?
2/7 - The Diagnosis I

💥Intravascular Lymphoma (IVL)💥

IVL can be an elusive diagnosis, given that many patients present without lymphadenopathy.

Instead, non-specific symptoms (e.g., fever, fatigue, weight loss, confusion) are more common.

ncbi.nlm.nih.gov/pmc/articles/P…Image
3/7 - The Diagnosis II

Some have resorted to random skin biopsies to make the diagnosis of IVL.

And multiple case series have demonstrated that a diagnosis of IVL can be made this way, even when the skin appears normal.

pubmed.ncbi.nlm.nih.gov/18053461/Image
Read 7 tweets
Jun 20, 2024
1/11
🤔Why does chronic hepatitis C infection "require" the intermediary of cirrhosis in order to cause hepatocellular carcinoma (HCC)?

Chronic hepatitis B can "skip" this step, going directly from chronic infection to HCC.

Why the difference?
2/
To begin, let's look at how frequently HCC occurs in patients without cirrhosis.

A 2019 study of United States (US) medical centers included 5144 patients with HCC.

💡12% had no underlying cirrhosis

pubmed.ncbi.nlm.nih.gov/31475372/
3/
A 2022 study found a similar rate, with 13% of patients with HCC showing no evidence of cirrhosis.

When looking more specifically at hepatitis C (HCV) versus hepatitis B (HBV), they found varying rates:

➣ HCV: 6% of patients with HCC were non-cirrhotic
➣ HBV: 19% of patients with HCC were non-cirrhotic

pubmed.ncbi.nlm.nih.gov/34027591/Image
Read 11 tweets
Apr 9, 2024
1/12 - Mystery #1

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.

ncbi.nlm.nih.gov/pmc/articles/P…Image
3/12 - An Initial Explanation (I)

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).

pubmed.ncbi.nlm.nih.gov/20609968/Image
Read 12 tweets
Feb 22, 2024
1/10
🤔Why is pulmonary embolism (PE) relatively rare in those with Factor V Leiden?

This Factor V Leiden Paradox was pointed out to me by @DrSamelsonJones after I posted about a similar difference with Behçet Syndrome.

Let's have a look.
2/
In 1993, Dahlback, Carlsson, and Svensson first described a heritable resistance to activated protein C.

A year later the same group found this to be the most common form of hereditary hypercoagulability.


ncbi.nlm.nih.gov/pmc/articles/P…
pubmed.ncbi.nlm.nih.gov/8302317/Image
Image
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.

Thus the name for the condition: Factor V Leiden.

pubmed.ncbi.nlm.nih.gov/8164741/Image
Read 10 tweets
Feb 18, 2024
1/8
🤔Why is pulmonary embolism (PE) so rare in Behçet Syndrome?

The condition is associated with a 14-fold increased risk of deep vein thrombosis (DVT) but almost none of these result in PE.

What is it about the thrombus in Behçet that makes it so unable to embolize?
2/
Numerous case series have reported a markedly increased risk of deep vein thrombosis with Behçet Syndrome.

One reported the following rates of venous thrombosis:
➣ Behçet Syndrome: 18/73 (25%)
➣ Controls: 4/146 (3%)

pubmed.ncbi.nlm.nih.gov/11426022/Image
3/
Another study of 882 patients with vascular Behçet Syndrome reported the following rates of deep vein thrombosis (DVT) and pulmonary embolism (PE):

➣ DVT: 592/882 (67%)
➣ PE: 0%!

pubmed.ncbi.nlm.nih.gov/24907156/Image
Read 9 tweets

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