❤️Bundle Branch Reentrant Tachycardia (BBRT) – A Rare but Important Ventricular Tachycardia⤵️
🔹Seen in patients with structural heart disease, especially dilated cardiomyopathy or post-surgical hearts.
🔹What is BBRT?
A macroreentrant VT that utilizes the His-Purkinje system as part of the reentry circuit.
It’s a form of ventricular tachycardia that mimics supraventricular origin on ECG due to its relatively narrow QRS (compared to other VTs).
🔹Mechanism:
- One bundle branch acts as the antegrade limb
- The other as the retrograde limb
- The circuit involves the interventricular septum
- Often associated with prolonged HV
🔹Seen in patients with structural heart disease, especially dilated cardiomyopathy or post-surgical hearts.
🔹What is BBRT?
A macroreentrant VT that utilizes the His-Purkinje system as part of the reentry circuit.
It’s a form of ventricular tachycardia that mimics supraventricular origin on ECG due to its relatively narrow QRS (compared to other VTs).
🔹Mechanism:
- One bundle branch acts as the antegrade limb
- The other as the retrograde limb
- The circuit involves the interventricular septum
- Often associated with prolonged HV
🔹ECG Findings (as in the image):
A. Type A BBRT with LBBB morphology → indicates antegrade conduction through the right bundle.
B. Type C BBRT with RBBB morphology + left axis deviation → indicates antegrade conduction through the left posterior fascicle.
🔹Clinical Significance:
- Can present as sustained monomorphic VT
- Often inducible during EP study
- May cause syncope, presyncope, or palpitations
- Frequently seen in patients with baseline bundle branch block and cardiomyopathy
🔹Treatment:
- Catheter ablation (typically of the RBB) is highly effective
- ICD may be considered if underlying cardiomyopathy is present
https://www.tg-me.com/cardiology
A. Type A BBRT with LBBB morphology → indicates antegrade conduction through the right bundle.
B. Type C BBRT with RBBB morphology + left axis deviation → indicates antegrade conduction through the left posterior fascicle.
🔹Clinical Significance:
- Can present as sustained monomorphic VT
- Often inducible during EP study
- May cause syncope, presyncope, or palpitations
- Frequently seen in patients with baseline bundle branch block and cardiomyopathy
🔹Treatment:
- Catheter ablation (typically of the RBB) is highly effective
- ICD may be considered if underlying cardiomyopathy is present
https://www.tg-me.com/cardiology
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Cardiology
👨💻 @dr_navruz
𝐂𝐨𝐫𝐨𝐧𝐚𝐫𝐲 𝐏𝐞𝐫𝐟𝐨𝐫𝐚𝐭𝐢𝐨𝐧 𝐜𝐥𝐚𝐬𝐬𝐢𝐟𝐢𝐜𝐚𝐭𝐢𝐨𝐧
Coronary perforations are best classified according to location, as location has important implications regarding management . There are three main perforation locations:
(1) large vessel perforation
(2) distal vessel perforation
(3) collateral vessel perforation, in either a septal or an epicardial collateral
Most coronary perforations (75% in one series) were large vessel perforations, followed by distal vessel perforation (25%)
The severity of coronary perforations has traditionally been graded using the 𝑬𝒍𝒍𝒊𝒔 𝒄𝒍𝒂𝒔𝒔𝒊𝒇𝒊𝒄𝒂𝒕𝒊𝒐𝒏
1. Class I: A crater extending outside the lumen only, in the absence of linear staining angiographically suggestive of
dissection.
2. Class II: Pericardial or myocardial blush without a more then 1 mm exit hole.
3. Class III: Frank streaming of contrast through a more then 1 mm exit hole.
4. Class III-cavity spilling: Perforation into an anatomic cavity chamber, such as the coronary sinus , theright ventricle, the left ventricle, etc.
Coronary perforations are best classified according to location, as location has important implications regarding management . There are three main perforation locations:
(1) large vessel perforation
(2) distal vessel perforation
(3) collateral vessel perforation, in either a septal or an epicardial collateral
Most coronary perforations (75% in one series) were large vessel perforations, followed by distal vessel perforation (25%)
The severity of coronary perforations has traditionally been graded using the 𝑬𝒍𝒍𝒊𝒔 𝒄𝒍𝒂𝒔𝒔𝒊𝒇𝒊𝒄𝒂𝒕𝒊𝒐𝒏
1. Class I: A crater extending outside the lumen only, in the absence of linear staining angiographically suggestive of
dissection.
2. Class II: Pericardial or myocardial blush without a more then 1 mm exit hole.
3. Class III: Frank streaming of contrast through a more then 1 mm exit hole.
4. Class III-cavity spilling: Perforation into an anatomic cavity chamber, such as the coronary sinus , theright ventricle, the left ventricle, etc.
Peripartum Cardiomyopathy (PPCM)
PPCM is an idiopathic cardiomyopathy with the following characteristics:
Development of heart failure (HF) toward the end of pregnancy or within five months following delivery.
Absence of another identifiable cause for the HF.
Left ventricular (LV) systolic dysfunction with LV ejection fraction (LVEF) of less than 45 percent. The LV may or may not be dilated.
Etiology:
The cause is uncertain, but potential aetiologies include inflammatory, angiogenic imbalance hormonal, hemodynamic, and autoimmune factors biologically active 16 kDa prolactin and other factors, such as soluble fms-like tyrosine kinase 1 (sFlt1), may initiate and drive PPCM
University study reveals that one of the possible primary causes of PPCM is a functional heart cell defect.
Dr. Naftali-Shani harnessed a cutting-edge genetic engineering technique, which won the Nobel Prize for medicine and physiology in 2012, to produce stem cells and beating heart cells from the skin cells of PPCM patients and healthy controls.
"This is the first time that this technique was used to study the mechanism of PPCM," Dr. Naftali-Shani says. . The myocardial cells produced from the stem cells of the patients had functional defects that caused them to secrete inflammatory proteins and a protein that inhibits the formation of blood vessels in the muscle, even without stress. We hope that this discovery will pave the way for early diagnoses and new, effective prevention and treatments.
Risk factors — Although the etiology of PPCM remains unclear, the following are among the factors associated with increased
risk of PPCM:
Age greater than 30 years.
African descent
Pregnancy with multiple fetuses
A history of preeclampsia, eclampsia, or postpartum hypertension
Maternal cocaine abuse
Long-term (>4 weeks) oral tocolytic therapy with beta-adrenergic agonists such as terbutaline
Although multiparity has been traditionally considered a risk factor for PPCM, studies have shown that the majority of patients who develop PPCM do so during the first or second pregnancy
There are conflicting data as to whether selenium deficiency is or is not a risk factor for PPCM.
Diagnosis.
Careful history taking is necessary to identify and exclude other causes of HF. The LV may be non-dilated, but the EF is usually <45%. Symptoms and signs are often typical for HF with numerous phenotypes reported. Patients frequently present with acute HF, but also with ventricular arrhythmias and/or cardiac arrest.
Echocardiography is the imaging modality of choice.
generally reveals a global reduction in LV systolic function with LVEF nearly always <45 percent . The LV is frequently but not always dilated . Other possible echocardiographic findings include left atrial enlargement, LV or left atrial thrombus, dilated right ventricle, right ventricular hypokinesis, mitral and tricuspid regurgitation, and small pericardial effusion
N.B Initial LVEF <30%, marked LV dilatation (LV end-diastolic diameter ≥6.0 cm), and RV involvement are associated with adverse outcomes
Recovery of left ventricular function
Partial or complete recovery of LV function is common among patients with PPCM and appears to be more frequent than with other types of dilated cardiomyopathy . Complete recovery of LV function (defined as recovery to an LVEF >50 percent) has been reported in 20 to 60 percent of patients in various series . Although nearly all recovery of LV function occurred within six months of diagnosis in some series , delayed recovery of LV function has been observed
Various studies have identified the following predictors of persistent LV dysfunction at follow-up:
LVEF ≤30 percent
Fractional shortening less than 20 percent and an LV end-diastolic dimension ≥6 cm
Black race
Reduced right ventricular function
MANAGEMENT
Treatment of peripartum cardiomyopathy (PPCM) is largely similar to treatment for other types of heart failure (HF).
PPCM is an idiopathic cardiomyopathy with the following characteristics:
Development of heart failure (HF) toward the end of pregnancy or within five months following delivery.
Absence of another identifiable cause for the HF.
Left ventricular (LV) systolic dysfunction with LV ejection fraction (LVEF) of less than 45 percent. The LV may or may not be dilated.
Etiology:
The cause is uncertain, but potential aetiologies include inflammatory, angiogenic imbalance hormonal, hemodynamic, and autoimmune factors biologically active 16 kDa prolactin and other factors, such as soluble fms-like tyrosine kinase 1 (sFlt1), may initiate and drive PPCM
University study reveals that one of the possible primary causes of PPCM is a functional heart cell defect.
Dr. Naftali-Shani harnessed a cutting-edge genetic engineering technique, which won the Nobel Prize for medicine and physiology in 2012, to produce stem cells and beating heart cells from the skin cells of PPCM patients and healthy controls.
"This is the first time that this technique was used to study the mechanism of PPCM," Dr. Naftali-Shani says. . The myocardial cells produced from the stem cells of the patients had functional defects that caused them to secrete inflammatory proteins and a protein that inhibits the formation of blood vessels in the muscle, even without stress. We hope that this discovery will pave the way for early diagnoses and new, effective prevention and treatments.
Risk factors — Although the etiology of PPCM remains unclear, the following are among the factors associated with increased
risk of PPCM:
Age greater than 30 years.
African descent
Pregnancy with multiple fetuses
A history of preeclampsia, eclampsia, or postpartum hypertension
Maternal cocaine abuse
Long-term (>4 weeks) oral tocolytic therapy with beta-adrenergic agonists such as terbutaline
Although multiparity has been traditionally considered a risk factor for PPCM, studies have shown that the majority of patients who develop PPCM do so during the first or second pregnancy
There are conflicting data as to whether selenium deficiency is or is not a risk factor for PPCM.
Diagnosis.
Careful history taking is necessary to identify and exclude other causes of HF. The LV may be non-dilated, but the EF is usually <45%. Symptoms and signs are often typical for HF with numerous phenotypes reported. Patients frequently present with acute HF, but also with ventricular arrhythmias and/or cardiac arrest.
Echocardiography is the imaging modality of choice.
generally reveals a global reduction in LV systolic function with LVEF nearly always <45 percent . The LV is frequently but not always dilated . Other possible echocardiographic findings include left atrial enlargement, LV or left atrial thrombus, dilated right ventricle, right ventricular hypokinesis, mitral and tricuspid regurgitation, and small pericardial effusion
N.B Initial LVEF <30%, marked LV dilatation (LV end-diastolic diameter ≥6.0 cm), and RV involvement are associated with adverse outcomes
Recovery of left ventricular function
Partial or complete recovery of LV function is common among patients with PPCM and appears to be more frequent than with other types of dilated cardiomyopathy . Complete recovery of LV function (defined as recovery to an LVEF >50 percent) has been reported in 20 to 60 percent of patients in various series . Although nearly all recovery of LV function occurred within six months of diagnosis in some series , delayed recovery of LV function has been observed
Various studies have identified the following predictors of persistent LV dysfunction at follow-up:
LVEF ≤30 percent
Fractional shortening less than 20 percent and an LV end-diastolic dimension ≥6 cm
Black race
Reduced right ventricular function
MANAGEMENT
Treatment of peripartum cardiomyopathy (PPCM) is largely similar to treatment for other types of heart failure (HF).
However, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, angiotensin receptor-neprilysin inhibitor, and aldosterone antagonists are to be avoided, as they are contraindicated in pregnancy.
HF with pulmonary congestion is treated with loop diuretics and thiazides if required; however, diuretics should be avoided in the absence of pulmonary congestion, due to the potential reduction in placental blood flow.
Hydralazine and nitrates appear safe in pregnancy, although with less evidence for benefit than ACE inhibitors, and should only be used in the presence of hypertension, severe LV dysfunction, and/or evidence of congestion in decompensated HF. Beta-blockers should be initiated cautiously and gradually uptitrated to the maximum tolerated dose
Additional therapeutic issues for this population may include arrhythmia management, anticoagulation therapy, mechanical support, and investigational therapies such as bromocriptine
Bromocriptine
The role of bromocriptine therapy in PPCM is controversial.
Addition of bromocriptine to standard HF therapy may improve LV recovery and clinical outcome in women with acute severe PPCM.
Bromocriptine (2.5 mg once daily) for at least 1 week may be considered in uncomplicated cases, whereas prolonged treatment (2.5 mg twice daily for 2 weeks, then 2.5 mg once daily for 6 weeks) may be considered in patients with EF <25% and/or cardiogenic shock. Bromocriptine treatment must always be accompanied by anticoagulation with heparin (LMWH or UFH), at least in prophylactic dosages
Decisions regarding the timing and mode of delivery in PPCM should be made based upon combined input from cardiology, obstetrics, anesthesiology, and neonatology services. Prompt delivery is suggested in women with PPCM with advanced HF.
All women with PPCM should receive counseling on the potential risk of recurrence with future pregnancies..
Peripartum cardiomyopathy(PPCM)
1-Defined as unexplained cardiomyopathy, EF less than 45% that occur in the last month of pregnancy or the first 5 months post partum
2-Pathphysiology is thought to be related to prolactin degradation product which has a myocardial toxcity which explain the benefit of anti-prolactin which is Bromocriptine
Other theories include autoimmune, myocarditis, oxidative stress
3-Predictors of poor prognosis include dilated LVEDD more than 60 mm, EF less than 30% and RV involvement
4-According to the ESC guidelines for heart disease with pregnancy, Bromocriptine is a class II b indication for PPCM
5-There are two regimens
I-Bromocriptine 2.5 mg once daily for 1 week
II-Bromocriptine 2.5 mg twice daily for 2 weeks then 2.5 mg once daily for 6 weeks
The first regimen for uncomplicated cases
The second regimen is used if the patient is presenting with cardiogenic shock or EF less than 25%
6-You must give parentral anticoagulation for patients on Bromocriptine(either prophylactic or therapeutic)
7-You must continue on antifailure measures for at least 6 months after recovery of normal LV function
8-Women who did not recover LV EF Above 50% should be prohibited from further pregnancies
9-Women who have recovered normal LV function still have a higher risk than those who did not have PPCM and risk of recurrence as well
10-Levosimendan is the inotrope of the choice due to deleterious effect of beta agonist on the heart by Catecholamines release
https://www.tg-me.com/cardiology
HF with pulmonary congestion is treated with loop diuretics and thiazides if required; however, diuretics should be avoided in the absence of pulmonary congestion, due to the potential reduction in placental blood flow.
Hydralazine and nitrates appear safe in pregnancy, although with less evidence for benefit than ACE inhibitors, and should only be used in the presence of hypertension, severe LV dysfunction, and/or evidence of congestion in decompensated HF. Beta-blockers should be initiated cautiously and gradually uptitrated to the maximum tolerated dose
Additional therapeutic issues for this population may include arrhythmia management, anticoagulation therapy, mechanical support, and investigational therapies such as bromocriptine
Bromocriptine
The role of bromocriptine therapy in PPCM is controversial.
Addition of bromocriptine to standard HF therapy may improve LV recovery and clinical outcome in women with acute severe PPCM.
Bromocriptine (2.5 mg once daily) for at least 1 week may be considered in uncomplicated cases, whereas prolonged treatment (2.5 mg twice daily for 2 weeks, then 2.5 mg once daily for 6 weeks) may be considered in patients with EF <25% and/or cardiogenic shock. Bromocriptine treatment must always be accompanied by anticoagulation with heparin (LMWH or UFH), at least in prophylactic dosages
Decisions regarding the timing and mode of delivery in PPCM should be made based upon combined input from cardiology, obstetrics, anesthesiology, and neonatology services. Prompt delivery is suggested in women with PPCM with advanced HF.
All women with PPCM should receive counseling on the potential risk of recurrence with future pregnancies..
Peripartum cardiomyopathy(PPCM)
1-Defined as unexplained cardiomyopathy, EF less than 45% that occur in the last month of pregnancy or the first 5 months post partum
2-Pathphysiology is thought to be related to prolactin degradation product which has a myocardial toxcity which explain the benefit of anti-prolactin which is Bromocriptine
Other theories include autoimmune, myocarditis, oxidative stress
3-Predictors of poor prognosis include dilated LVEDD more than 60 mm, EF less than 30% and RV involvement
4-According to the ESC guidelines for heart disease with pregnancy, Bromocriptine is a class II b indication for PPCM
5-There are two regimens
I-Bromocriptine 2.5 mg once daily for 1 week
II-Bromocriptine 2.5 mg twice daily for 2 weeks then 2.5 mg once daily for 6 weeks
The first regimen for uncomplicated cases
The second regimen is used if the patient is presenting with cardiogenic shock or EF less than 25%
6-You must give parentral anticoagulation for patients on Bromocriptine(either prophylactic or therapeutic)
7-You must continue on antifailure measures for at least 6 months after recovery of normal LV function
8-Women who did not recover LV EF Above 50% should be prohibited from further pregnancies
9-Women who have recovered normal LV function still have a higher risk than those who did not have PPCM and risk of recurrence as well
10-Levosimendan is the inotrope of the choice due to deleterious effect of beta agonist on the heart by Catecholamines release
https://www.tg-me.com/cardiology
Telegram
Cardiology
👨💻 @dr_navruz