cardiovascular remodeling and it's prevention
DESCRIPTION
cardiovascular remodeling and it's prevention,hypertension,anti hypertensive drugsTRANSCRIPT
Good Afternoon
ROLE OF DRUGS IN PREVENTING THE
REMODELING OF CARDIOVASCULAR
SYSTEM IN FOLLOW UP OF HF PATIENT
ROLE OF DRUGS IN PREVENTING THE
REMODELING OF CARDIOVASCULAR SYSTEM IN FOLLOW UP OF HF PATIENT
PRESENTED BY- SUBRATA DAS
ASISH BARUI
Definition- This is a clinico-pathological condition in whichheart cannot maintain adequate cardiac output to meet theMetabolic demand of the tissue in response to normal venous reterurn
HEART FAILURE
• Cardiac injury –> depressed cardiac function poor tissue perfusion
• Cardiac output must increase– Activation of neurohormonal axis– Norepi, AVP, angiotensin II, endothelin
• Chronic NH release is dysfunctional– Alterations in HR, contractility– Myocardial hypertrophy and ischemia
PATHOPHYSIOLOGY
Neurohormonal changes
CHF Vicious Cycle
LOW CARDIAC OUT PUT
Increased Preload Increased Aft erload Norepinephrine
Increased Salt Vasoconstricti on Renal Blood Flow
ReninAngiotension IAngiotension IIAldosterone
Circulating and local (tissue) RAS influence on the cardiovascular system
Circulating RASShort-term effects
Sodium/water reabsorption via aldosterone secretion
Local RASLong-term effects
Intraglomerular hypertension
Vascular hypertrophyby Increase production of
growth factors &extracellular matrix
HeartHeart
VasoconstrictionPositive chronotropic effects/ arrhythmogenic effects
Myocardial hypertrophy
ANGIOTENSIN II
BradykininAngiotensin I
Angiotensin IIACE inhibitor
AT1-blocker
VasodilatationNatriuresisExtracellular matrix degradationAngioedema
HypertensionAldosteroneTransforming growth factor Plasminogen activator
AT1Receptor AT2Receptor
Sympathetic stimulation
•Myocyte apoptosis•Hypertrophy•Focal myocardial necrosis
-blocker
Angiotesinogen
Renal hypoxia
Central Sympathetic stimulation
-blocker
Reduced cardiac output
Myocardial inadequacy
Cardiovascular remodeling
Digitalis
ACE INHIBITORs• ACE inhibitors interfere with the renin-
angiotensin system by inhibiting the enzyme that is responsible for the conversion of angiotensin I to angiotensin II.
• However, because ACE inhibitors also inhibit kininase II, they may lead to the upregulation of bradykinin, which may further enhance the beneficial effects of angiotensin suppression.
• ACE inhibitors stabilize LV remodeling, improve symptoms, reduce hospitalization, and prolong life
DRUGS & DOSE
Angiotensin-converting enzyme inhibitor
Initiating Dose Maximal Dose
Captopril 6.25 mg tid 50 mg tid
Enalapril 2.5 mg bid 10 mg bid
Lisinopril 2.5–5.0 mg qd 20–35 mg qd
Ramipril 1.25–2.5 mg bid 2.5–5 mg bid
Trandolapril 0.5 mg qd 4 mg qd
Angiotensin-converting enzyme inhibitor
Initiating Dose
Maximal Dose
Captopril 6.25 mg tid 50 mg tid
Enalapril 2.5 mg bid 10 mg bid
Lisinopril 2.5–5.0 mg qd 20–35 mg qd
Ramipril 1.25–2.5 mg bid 2.5–5 mg bid
Trandolapril 0.5 mg qd 4 mg qd
β BLOCKERS•Beta blocker block central sympathetic stimulation which activate the RAS & sympathetic stimulation by angiotensin II
•The beneficial affect due to antagonism of ventricular wall stress enhancing, apoptosis promoting and pathological remodeling effects of excess sympathetic activity
•It improve patient symptoms, prevent hospitalization, and prolong life
•The only contraindication is severe decompensate CHFCarvedilol 3.125 mg bid
Bisoprolol 1.25 mg qd
Metoprolol succinate CR 12.5–25 mg qd
DigitalisMechanism of Action
• +ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase → inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange
• Vagotonic effect• Arrhythmogenic effect
Drug Initial dose Maintenance dose
Digoxin Tab 0.25 mg -4 tab stat. Tab 0.25 mg -1/2 to 1 tab daily
CONCLUSION
A. Myocardial & vascular remodeling is sing of progressive heart failure
B. Prevention of remodeling is proven benefit using ACE inhibitor, beta blocker & digitalis.
Thank You….
QUESTIONS?