The Heart

Poor R Wave Progression (PRWP) ECG

🫀Normal R-wave height in V3 is usually greater than 2 mm i.e 3 mm or more
if the height of the r wave in leads V1 to V4 remains extremely small, we say there is "poor R-wave progression"

🫀Commonly attributed to a previous anterior myocardial infarction
🫀A number of other conditions result in a - poor R wave progression
for example left bundle branch block, left anterior fascicular block, Wolff-Parkinson-White syndrome, certain types of right ventricular hypertrophy (especially that associated with chronic pulmonary disease), and left ventricular hypertrophy all may result in poor R wave progression

🫀less common causes of poor Rwave progression include spontaneous pneumothorax, corrected transposition of the great vessels and congenital absence of the pericardium

🫀Poor R wave progression secondary to previous anterior myocardial infarction
in anterior myocardial infarctions, this produces Q waves in the right and midprecordial leads (V1-V4)however, in a significant number of patients the Q waves do not persist with previously documented anterior myocardial infarction, the reported estimate of poor Rwave progression on subsequent ECGs varies between 20% and 30%
🫀Average length of time for the complete disappearance of the abnormal Q waves is 1.5 years
🫀 The magnitude of the subsequent leftward forces is less than in patients with poor Rwave progression from other causes
https://ecg-educator.blogspot.com/2016/02/r-wave-progression.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771797/

https://twitter.com/LearntheHeart/status/990481168595345408/photo/1

Wellen's Syndrome : Type A and Type B

Wellens' Syndrome on ECG
▶️Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery.

▶️Diagnostic criteria for Wellens’ syndrome on ECG are:
1) Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6).
2) Isoelectric or minimally-elevated ST segment (< 1mm).
3) No precordial Q waves,
4) Preserved precordial R wave progression.

▶️There are two patterns of T-wave abnormality in Wellens’ syndrome:
1) Type A = Biphasic, with initial positivity & terminal negativity (25% of cases),
2) Type B = Deeply and symmetrically inverted (75% of cases).

The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction

https://www.sciencedirect.com/science/article/abs/pii/S0735675708004816

Critical Care Management of the Patient With
Anaphylaxis: A Concise Definitive Review

https://journals.lww.com/ccmjournal/abstract/2021/05000/critical_care_management_of_the_patient_with.12.aspx

Antithrombotic therapy in patients with acute coronary syndrome:
👉Similarities & differences between a European expert consensus document and the 2023 ESC guidelines
https://academic.oup.com/ehjacc/advance-article-abstract/doi/10.1093/ehjacc/zuad158/7505515?redirectedFrom=fulltext&login=false

Albumin administration in internal medicine: A journey between effectiveness and futility


https://www.ejinme.com/article/S0953-6205(23)00232-7/fulltext?s=09

Brilliant Summary on Aortic Valve Calcium Score CT/CMR Lecture by

💥Important to begin by appreciating burden of AS.
💥 remains primary modality to assess HEMODYNAMIC severity.
💥Need other tools to assess ANATOMIC severity!

💥JACC 2019➡️Review non-contrast CT to measure AVC in AS.
💥An example protocol ⬇️ measuring calcium burden in en-face view of AV.
💥Pitfalls: inclusion of LVOT, sorta, mitral annulus & cors. Multi-planar reconstruction helps carefully exclude non-AV calcium.

💥Women & Men are different! For a given amount of AVC, 🚺 have a ⬆️ peak jet vel. by . For a given peak vel. by 🚹 have higher iAVC.
💥AVCd didn’t help resolve the discordance.
💥2017 ESC guidelines for severe AVC ➡️>1200 AU 🚺,>2000AU🚹.

💥Reason for s*x disparity was recognized as being ⬆️ fibrosis in 🚺 compared to 🚹
💥In young patients w/ bicuspid AV(YBAV) ⬆️HEMODYNAMIC severity of AS was found in absence of significant AVC.
💥YBAV usually identified by alone.Older pts w/ LFLG benefit from

💥But does our knowledge of ANATOMIC severity of AVC w/ impact outcomes?
💥YES ⬇️ severe AVC at baseline predicts outcome (survival) as well as rate of progression.

💥Moving on to using AVC as a tie-breaker in low-gradient AS. Beautifully outlined below.

A-D-E-N-O-S-I-N-E .
💊Adenosine (or adenosine like molecules) are agents we use in cardiology regularly. Adenosine is a natural molecule found in our cells that assists with multiple biological process such as energy transfer (ATP and ADP) as well as cellular signaling (cAMP). Who said biochemistry wasn’t important! .
💝In cardiology most people usually think of adenosine as the agent we give in patient with supraventricular tacycardia. Additional places we use adenosine are in the nuclear stress lab (for stress/vasodilator perfusion studies) and in the Cath lab (for coronary no reflow, SVG interventions, and pulmonary HTN vasoreactivity challenges).
💡All of these things make sense if you understand what adenosine does in the body. The above picture shows adenosine and it’s four receptors: .
1️⃣A1 - Causes AV block
2️⃣A2A - Causes Coronary vasodilation .
3️⃣A2B - Causes Bronchospasm peripheral vasodilation .
4️⃣A3- Causes Bronchospasm .
🤢Often times adenosine also causes a variety of other side effects like flushing, headache, shortness of breath, hypotension, etc. Patients will nearly always experience some sort of side effect but luckily the half life of adenosine (10 sec) is so short these are usually self resolving. Sometimes we give nonselective adenosine competitive antagonists like aminophylline and caffeine to reverse the effects. .
👀Be on the look out for these agents! Even though we always think of adenosine for SVT remember the other places it’s used (or a derivative), which in the hospital, is most likely in the nuclear stress lab! .Excellent summary by Dr Jay Mohan

AORTIC REGURGITATION OVERVIEW

Tips and Tricks in Echocardiography

from Tips and Tricks in Cardiology book
By Ahmed Mohsen

Carotid Plaque-RADS Scores: Stroke risk classification system

The multidisciplinary-derived carotid Plaque-RADS score is a novel risk classification system; may reshape therapeutic decisions via consistent plaque imaging and reporting. bit.ly/3O5KtO5

Management of patients hospitalized for acute heart failure: 2023
Pre-discharge and early post-discharge
a scientific statement by the Heart Failure Association (HFA) of the ESC
https://onlinelibrary.wiley.com/doi/abs/10.1002/ejhf.2888

Acute coronary syndromes and acute heart failure: a diagnostic dilemma and high-risk combination. A statement from the AHF Committee of the HFA of the ESC
https://onlinelibrary.wiley.com/doi/full/10.1002/ejhf.1831

STEMI Mimics

https://rydestation.wordpress.com/2014/11/20/stemi-mimics/

Timeline of Complications:Early and Late Complications of Acute - MI
=====////======/////=====////====

- Ventricular Arrhythmias
- Bradyarrhythmias / Heart Block
- Cardiogenic Shock
- Stroke
- Ischemic MR / Papillary Muscle Rupture
- Ventricular Septal Rupture
- LV Free Wall Rupture
- Pericarditis (Dressler Syndrome)

🫀Ventricular tachycardia and ventricular fibrillation may occur any time after the coronary artery is occluded. These arrhythmias, which are due to ischemia, are particularly common during the first few hours after artery occlusion. They cause the vast majority of deaths in the acute phase. The risk then rapidly abates within 6 hours.

🫀However, myocardial infarction (particularly if extensive and in presence of heart failure) may result in chronic remodeling of the myocardium; such remodeling can cause ventricular tachycardia and ventricular fibrillation.

🫀The most common mechanical complication of acute STEMI (and myocardial infarction in general) is papillary muscle rupture. Wall rupture (septum or left ventricular free wall) is less common.

🫀Ischemic bradyarrhythmia (bradycardia) is also common, especially with inferior infarctions.
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)30677-8/fulltext

📌Integration of implantable device therapy in patients with heart failure
A clinical consensus 📝 from the & of the

https://onlinelibrary.wiley.com/doi/10.1002/ejhf.3150

Takotsubo syndrome: between evidence, myths, and misunderstandings

https://link.springer.com/article/10.1007/s00059-020-04906-2

OMI: Replacing the STEMI misnomer
What’s wrong with the STEMI label?
What is an OMI?

🫀Occlusion Myocardial Infarction (OMI): A branch of the ACS algorithm representing near or total occlusion with insufficient collateral circulation causing active infarction

🫀Non-Occlusion Myocardial Infarction (NOMI): No occlusion, or sufficient collateral circulation to avoid active infarction

https://litfl.com/omi-replacing-the-stemi-misnomer/

23 years old male with upper respiratory tract infection and severe localizaed chest pain increased with breathing. ECG 1 & 2 are shown. PLease check the timing .
What is the Diagnosis ?


ECG courtesy of Dr ihab sulimman

39 Years old .
Routine . What is the diagnosis ?

Time to Quadruple Guideline-Directed Medical Therapy for Heart Failure
🏨 with HFrEF

Only one at a time
Go slow
Defer to outpatient
Be cautious

What is the worst that can happen?

Delay ARNI ➡️ 42% ⬆️ risk CV☠️/HF🏨
Delay BB ➡️ 25% ⬆️ risk ☠️
Delay MRA ➡️ 37% ⬆️ risk CV☠️/HF🏨
Delay SGLTi ➡️ 58% ⬆️ risk CV☠️/HF🏨/ER

Urgency needed!

If following a historical sequential approach to GDMT +

⚠️ only making 💊 changes during f/u visits

⚠️ seeing patients back at 3 months intervals

🤯 it would take 14 x 3 months = 42 months (3.5 years) before quadruple GDMT would be achieved

Don’t delay!

https://onlinejcf.com/article/S1071-9164(23)00069-6/fulltext

Top stories on Brugada syndrome :
🫀Progression of structural abnormalities in BrS over time
🫀Structural abnormalities in BrS are not limited to the RVOT
🫀Ablation of areas with structural abnormalities prevents ventricular fibrillation recurrence
🫀Role of the sodium channel blocker challenge test in the diagnosis of BrS
🫀New risk prediction score in BrS
https://www.heartrhythmjournal.com/article/S1547-5271(23)02773-X/fulltext

Approach for patients with Coronary artery disease (CAD) and thrombocytopenia
Summary By Ahmed Mohsen
=====/////=====/////=====/////=====//////
1-This is one of the most challenging situations in cardiology practice that needs alot of wisdom and precautions

2-To approach these patients we have to go through 2 parallel tracks:

-Thrombocytopenia track
-CAD track

I-Thrombocytopenia track:

1-What is the severity of thrombocytopenia?

Mild: Platelets count 150.000 to 100.000
Moderate :Platelets count 100.000 to 50.000
Severe : Platelets count less than 50.000

2-What is cause of thrombocytopenia?

If the etiology is malignancy, then what is the prognosis and life expectancy.
(malignancy with expected survival less than 1 year, mostly we will adopt conservative strategy)

3-Is there treatment for thrombocytopenia?

Can we increase the platelet count by certain drugs(eg:thrombopoitin agonist)
Or by treating the underlying condition( eg: Steroids in autoimmune disease)

II- Coronary artery disease track:

1-What is the clinical presentation?

A-Stable CAD : conservative

B- Low risk non ST elevation ACS: conservative

C-STEMI or high risk Non ST elevation ACS: invasive strategy

2-Antithrombotics:

You can use antiplatelet therapy if platelets count above 50 000

3-Strategy :
If platelets count above 50 000 and there is strong indication for invasive strategy (STEMI or high risk non ST elevation ACS) follow the following steps:

A-Radial access

B- Use Biofreedom stent to give DAPT only for 1 month then P2Y12 inhibitor monotherapy

C-Clopidogrel is the P2Y12 inhibitor of the choice

D-Use PPI
E- in Cath lab, Heparin dose can be reduced to 50 unit /kg

F-Avoid use of Glycoprotein IIb III ai

The management of antiplatelet therapy in acute coronary syndrome patients with thrombocytopenia: A clinical conundrum

https://www.researchgate.net/publication/320354286_The_management_of_antiplatelet_therapy_in_acute_coronary_syndrome_patients_with_thrombocytopenia_A_clinical_conundrum

Statins for all patients with HIV? A practice changing trial that brings CV health to the forefront of HIV therapy. REPRIEVE Trial, NEJM 2023 ♥️

💥Original Article: Pitavastatin to Prevent Cardiovascular Disease in People with HIV (REPRIEVE trial) nej.md/44PX1Pr

💥Editorial: HIV and Cardiovascular Disease: An Ounce of Prevention nej.md/3K8h183

Right Ventricular Involvement ECG signs in Myocardial Infarction

Pdf👉https://clinicalview.gehealthcare.com/poster/right-ventricular-involvement-ecg

Electrical and structural remodelling in female athlete's heart:
A comparative study in women vs men athletes and controls
https://www.sciencedirect.com/science/article/abs/pii/S0167527324001736?dgcid=author

HYPERKALEMIA MANAGEMENT

From Clinical Decision in critical care book

Book cover page and author in the comment section

Chronic Heart Failure: Approach, Evaluation and Management

https://manualofmedicine.com/topics/cardiology/chronic-heart-failure-approach-evaluation-management/

Medical Management and Device-Based Therapies in Chronic Heart Failure

https://www.sciencedirect.com/science/article/pii/S2772930323012085