Cardiovascular Education

Tetanus is a rare but life-threatening disease caused by the bacterium Clostridium tetani. Tetanus is acquired when C tetani from soil, dust, or manure enter the body through broken skin from puncture wounds, cuts, or burns.

In the human body, C tetani grows in damaged tissue and produces tetanus toxin, which travels to the central nervous system and blocks the release of neurotransmitters in the brain and spinal cord.

From 2013 to 2023, the US Centers for Disease Control (CDC) reported 267 cases of tetanus in the US, including 13 deaths.

📄This JAMA Patient Page describes the signs and symptoms of , the risk factors, vaccinations for prevention, and how it is diagnosed and treated.

https://ja.ma/4gyBL8u

CARDIOVASCULAR DISEASES IN PREGNANCY COMPILED FROM MY NOTES MADE FROM DIFFERENT UPDATED GUIDELINES 🤰🫀⚕👨‍⚕️🩺Educational note: This series is intended for cardiovascular education and should not replace individualized management by a Pregnancy Heart Team.

📚 References

European Society of Cardiology. 2025 European Society of Cardiology Guidelines for the Management of Cardiovascular Disease and Pregnancy. European Heart Journal. 2025.

Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, et al. 2018 European Society of Cardiology Guidelines for the management of cardiovascular diseases during pregnancy. European Heart Journal. 2018;39:3165–3241.

American College of Obstetricians and Gynecologists. Pregnancy and Heart Disease. Practice Bulletin Number 212. Obstetrics & Gynecology. 2019.

American College of Obstetricians and Gynecologists. Gestational Hypertension and Preeclampsia. Practice Bulletin Number 222. Obstetrics & Gynecology. 2020.

Mehta LS, Warnes CA, Bradley E, et al. Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association. Circulation. 2020.

Otto CM, Nishimura RA, Bonow RO, et al. 2020 American College of Cardiology/American Heart Association Guideline for the Management of Patients With Valvular Heart Disease. Circulation. 2021.

Elkayam U, Goland S, Pieper PG, Silverside CK. High-Risk Cardiac Disease in Pregnancy: Part I and Part II. Journal of the American College of Cardiology. 2016.

Davis MB, Arany Z, McNamara DM, Goland S, Elkayam U. Peripartum Cardiomyopathy: Journal of the American College of Cardiology State-of-the-Art Review. Journal of the American College of Cardiology. 2020.

European Society of Cardiology and European Heart Rhythm Association guidance on cardiac arrhythmias and antiarrhythmic therapy during pregnancy.

United States Food and Drug Administration. Pregnancy and Lactation Labeling Rule — prescribing information for pregnancy, lactation and reproductive potential.

🫀 ESC Congress 2026: Practice-Changing Updates in Cardiology

A domain-by-domain summary of the highest-yield, practice-changing messages from the ESC Congress 2026 cycle.

Coronary Artery Disease, ACS & Antithrombotics

🔹 Omit beta-blockers post-MI when LVEF ≥50%. REBOOT and an individual-patient-data meta-analysis showed no benefit for death, MI, or HF, with a possible harm signal in women. Beta-blockers should still be considered when LVEF is 40–49%, where benefit persists.
🔹 Abbreviated DAPT followed by P2Y12 monotherapy is emerging as the preferred strategy in uncomplicated, completely revascularized AMI. One month of DAPT reduced major bleeding by approximately half without an ischemic penalty in TARGET-FIRST. Avoid very early aspirin withdrawal (days 0–4), and clopidogrel monotherapy should not automatically be assumed to be the optimal P2Y12 strategy.
🔹 Consider extending DAPT beyond 12 months in higher-risk patients with multivessel disease who complete the first year event-free. However, remember that the Extended DAPT population was predominantly nonelderly and treated with clopidogrel.
🔹 AF + OAC + previous PCI: beyond 12 months after PCI in stable chronic coronary syndrome, drop the antiplatelet when appropriate. OAC monotherapy reduces bleeding without an apparent MACE penalty.
🔹 Intravascular imaging remains important for complex PCI, particularly left main and bifurcation interventions. Routine IVUS showed less incremental benefit in IVUS-CHIP, but its value remains clearest in anatomically complex PCI.

❤️ Heart Failure

🔹 HFpEF/HFmrEF therapy should increasingly be built around SGLT2 inhibition + finerenone, with an incretin such as semaglutide or tirzepatide added when obesity is present.
🔹 Digitalis has renewed evidence. DIGIT-HF showed that digitoxin reduced death/HF hospitalization in advanced HFrEF, while the DECISION withdrawal data raised concern about stopping established digoxin therapy.
🔹 Vericiguat: VICTOR missed its primary endpoint but demonstrated a nominal mortality signal, supported by pooled VICTORIA + VICTOR analyses.
🔹 TEER is expanding beyond the classic COAPT population. RESHAPE-HF2 supports TEER in appropriately selected patients with moderate-to-severe functional MR, with an NNT of approximately 5 for its primary clinical outcome.

🩸 Lipids & Prevention

🔹 PCSK9 inhibition is moving into high-risk primary prevention. VESALIUS-CV showed that evolocumab reduced MACE in patients without previous MI or stroke, including a substantial benefit in patients with diabetes without known atherosclerosis.
🔹 Measure Lp(a) once in every adult. Lp(a) is increasingly becoming part of routine lifetime cardiovascular risk assessment. The upcoming Lp(a)HORIZON/pelacarsen outcome data will be important for determining whether directly lowering Lp(a) translates into fewer cardiovascular events.
🔹 Target SBP

Practice Guideline ARNI

The American College of Cardiology (with the AHA and HFSA) recommends an ARNI, ACEi, or ARB to reduce morbidity and mortality in chronic HFrEF, and specifically recommends transitioning patients with NYHA class II–III symptoms who tolerate an ACEi or ARB to an ARNI to further reduce morbidity and mortality (Class I, LOE B-R).

The ARNI is preferred because it was tested head-to-head against a proven ACEi and won: in PARADIGM-HF, sacubitril/valsartan reduced the composite of cardiovascular death or HF hospitalization by 20% relative to enalapril, with an absolute 4.7% reduction and a number-needed-to-treat of 21 over 27 months, including a 20% reduction in sudden cardiac death.

Practical points from the guideline pathway:

- A 36-hour washout is required only when switching between an ACEi and an ARNI (to avoid additive angioedema risk); this is not required when switching from an ARB.

- ARNI can be started de novo in ACEi/ARB-naïve patients, including before hospital discharge in acute HFrEF, with efficacy and safety similar to treatment-experienced patients (PIONEER-HF, TRANSITION).

- A low-dose ARB first, then a switch to sacubitril/valsartan, is offered as an option only for patients with less robust blood pressure, not as a routine bridge for everyone.

The mortality evidence for ARNIs is direct head-to-head evidence, not old ACEi data extrapolated to a newer drug. This is the crux of the confusion. PARADIGM-HF randomized ambulatory HFrEF patients (LVEF ≤40%, later ≤35%) to sacubitril/valsartan versus enalapril—a full-dose, mortality-proven ACEi—on top of otherwise optimal therapy (beta-blocker, MRA in ~50%). The ARNI reduced all-cause mortality from 19.8% to 17.0% (HR 0.80, 95% CI 0.71–0.89) and cardiovascular death by the same margin.[4][5] So ARNI superiority was established after ARNIs existed, by beating the ACEi standard in a modern trial—not before.

The historical ACEi mortality trials (SOLVD, CONSENSUS, etc.) came decades earlier and established ACEi as the benchmark. ARNI then had to be built and tested against that benchmark. The natriuretic peptide pathway is why the combination outperforms an ACEi alone: neprilysin inhibition preserves natriuretic peptides, bradykinin, and other vasoactive peptides, adding benefit on top of RAAS blockade.

Why not just put everyone on an ARB to make the eventual ARNI switch easier? Several reasons make this a poor strategy:

- ARBs are not superior to ACEis—they are essentially equivalent, and are positioned as the alternative for ACEi-intolerant patients (cough or angioedema), not as a preferred first agent. Choosing an ARB "just in case" would mean choosing a drug with no mortality advantage over the alternatives when a superior option (ARNI) already exists.

- There is no need to bridge through an ARB at all. Guidelines endorse starting an ARNI de novo, including in hospitalized and treatment-naïve patients, so the "easier switch later" rationale does not hold—the ARNI can simply be the initial agent when blood pressure and eGFR (≥30 mL/min/1.73 m²) permit.

- The washout concern that ARBs would avoid is minor and specific. The 36-hour washout applies only to ACEi↔ARNI transitions; switching ARB→ARNI needs no washout. But this small convenience does not justify placing patients on a non-superior drug when the ARNI itself is the goal.[7]

- Delaying ARNI (or a proven ACEi) to sit on an ARB withholds the incremental mortality and HF-hospitalization benefit that PARADIGM-HF demonstrated. In HFrEF, achieving the best-evidence therapy promptly matters, so the field moves patients toward ARNI rather than parking them on ARBs.

The bottom line: the preferred sequence is to get patients onto an ARNI—either directly or by converting from an ACEi/ARB once tolerated—because that is the therapy with the strongest head-to-head mortality evidence. An ARB is a fallback for intolerance, not a strategic waystation.

In HCm patients initial medical therapy is betablockers to reduce myocardial o2 consumption and lower the outflow gradient in patients with dynamic obstruction.....

Diuretics should be generally avoided or administrated carefully in patients with HCM to prevent intravascular volume depletion and intensification of the outflow gradient....

Digoxshould be avoided in HCM in the absence of systolic dysfunction...increased ionotropic effect could exacerbate the LV outflow gradient...

HCM IS NOT AN INDICATION FOR ROUTINE ANTIBIOTICS PROPHYLAXIS

In patients with atrial fibrillation (AF), catheter ablation (CA) reduces the frequency of AF but does not prevent stroke caused by thromboembolism, so patients undergoing CA generally require continued long-term anticoagulation.

🍁🍁All ACEIs and ARBs are absolutely contraindicated in pregnancy and lactation, with the exception of captopril , enalapril and benzapril which can be given to nursing mothers .

Prefer them especially in postpartum cardiomyopathy lactating moms as SACUBATRIL/VALSARTAN TOO CONTRAINDICATED DURING LACTATION

IMPORTANT PRECAUTIONS WHILE USING ACEI & ARBS

Important practical drug remarks .
🛑🛑Never combine ACEI and ARB .

🛑🛑 You can use ACEI and ARBs safely in dialysis patients.

🛑🛑 Most ACEIs are prodrugs , so caution in patients with significant hepatic dysfunction . Only Captopril and lisinopril are active drugs.

🛑🛑All ACEIs and ARBs are absolutely contraindicated in pregnancy and lactation, with the exception of captopril , enalapril and benzapril which can be given to nursing mothers .

🛑🛑You can reach with ramipril up to 20 mg , specially in Proteinuria patients .

🛑🛑Still ACEIs over ARBs are 1st line treatment for improving outcome after MI .

🛑🛑Caution should be exercised when ACEIs or ARBs are used in combination with loop diuretics or metolazone . Excess diuresis , with hypovolemia and hyponatremia may be detrimental in deterioration of renal function .


🛑🛑 Take care from leucopenia while using captopril .Stop the drug and monitor the patient.

🛑🛑 Never combine ACEIs or ARBs with Aliskirin .

🛑🛑Take care from Unilateral eyelid or facial edema with ACEIs or ARBs , as it may be warning sign for angioneurotic edema .

🛑🛑 50% increase in s creatinine is a cutoff value to reduce dose or hold ACEI or ARB.

🛑Sudden Cardiac Death

🍁🍁Sudden cardiac death (SCD) is defined as sudden and unexpected death occurring within an hour from the onset of symptoms or occurring in patients found dead within 24 hours of being asymptomatic and presumably due to cardiac arrhythmia or hemodynamic catastrophe (2017 ACC guidelines for management of ventricular arrhythmia and prevention of sudden cardiac death).

🫀Causes above the age of 35 years:
🌸🌸SCD may occur as result of
Coronary artery disease
Hypertrophic cardiomyopathy or
Valvular heart disease.

🫀Causes below the age of 35 years:
🌸🌸Hypertrophic cardiomyopathy (usually without obstruction) is the commonest cause.
🌸🌸Congenital coronary anomalies (most often origin of left main coronary artery from right sinus of Valsalva).
🌸🌸Valvular heart disease (aortic stenosis, mitral valve prolapse).
🌸🌸Dilated cardiomyopathy
🌸🌸 Arrhythmogenic right ventricular cardiomyopathy.
🌸🌸Myocarditis.
🌸🌸Marfan syndrome (aortic rupture).
🌸🌸Premature coronary atherosclerosis.
🌸🌸Long QT syndrome, Brugada syndrome, WPW syndrome.
🌸🌸Catecholaminergic polymorphic ventricular tachycardia (CPVT)
🌸🌸, Idiopathic VT.
🌸🌸- Arrhythmias due to substance abuse with co***ne, anabolic steroids or ephedrine containing components.

🍁🍁Contraindications to MRI

🛑Automatic implantable cardioverter-defibrillator

🛑Cerebral aneurysm clips

🛑Iron containing foreign body in the eye that has been for more than 6 years

🛑Spinal cord stimulation devices

‼️‼️Note that coronary stents..heart valves...artificial joints and Vertebral plates not Contraindications to MRI

👉👉Mechanical cardiac valves..the c ring support structures for the tissue valves...coronary stents are made of non ferrous materials and are not contraindications to MRI....

However if there is a question of valve dehiscence then MRI is relatively contraindicated...

🛑Ppm tpm and icd are contraindications to MRI