Cardiovascular health Flashcards
Which DM drugs have been found to reduce MACE (major adverse cardiovascular event) and CV mortality?
- GLP1-RA
- SGLT2i: also decreased heart failure and decreased CV death for HFrF patients (regardless of if patient doesn’t have DM)
What is recommended drug therapy for ASCVD/indicators of high risk, HF, CKD with DM?
What is the role of lipoproteins in atherogenesis?
HDL involved with downregulating oxidative modification of LDL which results in formation of fatty streak in endothelium
What are the therapies to lower LDL-C?
What is the MoA of statins?
How can it be used as secondary prevention?
- Statins are HMG CoA reductase inhibiotrs: hence decreasing synthesis of cholesterol which lowers intracellular cholesterol –> stimulates upregulation of the LDLr and increases uptake of non-HDL particles from the systemic circulation
Secondary prevention:
* Scandinavian simvastatin survival study: statin treatment significantly reduces CV events in patients with ACS and no hypercholesterolemia.
* Statins reduces CV events in patients at high risk of CAD across a wide range of baseline LDL-C
* High dose statin significantly reduces CV evnets compared with low dose statin in chronic CHD patients
What is the MoA of PCSK9 inhibitors in hypercholesterolemia?
What is safety concerns and efficacy?
PCSK9 binds to LDLR on liver cell surface and mediates lysosomal degradation of the complex formed by PCSK9-LDLR-LDL.
In the presence of a monoclonal antibody (evolomumab) that binds to PCSK9, the PCSK9 mediated degradation of LDLr is inhibited, resulting in an increased uptake of LDLchoesterol by LDLR as more LDLR are recycles at the cell surace.
Safety concerns
* Risk of neurocognitive AE
* Risk of rhabdomyolysis
* Risk of liver enzyme elevations
* Risk of new onset DM
* Risk of allergic reaction
Efficacy
* Decrease relative risk of MI
* Decrease relative risk of ischemic stroke
* Decrease relative risk of coronary revascularization
What BP measurement used for dx of hypertension?
ABPM is a better predictor of clinical outcomes than clinic BP
Reference stsandard used in clinical practise when there is uncertainty about the dx
Improves the specificity and sensitivity of dx vs clinic and home BP measurement
What is treatment guideline for controlling hypertension?
What is the ATP 3 criteria for metabolic syndrome?
3 of the following 5 traits
* Abd obesity: waist circumference in men >102cm and in women >88cm
* Hypertriglyceridemia: serum triglycerides >1.7 mmol/L or drug treatment for elevated TG
* Reduced HDL: serum HDL cholesterol <1mmol/L in men and <1.3 mmol/L in women
* Increased BP: BP>130/85mmHg or drug treatmetn for elevated BP
* Increased glucose: fasting plasma glucose (FPG) >5.6mmol/L
What are the goals for BP and LDLc in step 1 (prevention goals) and step 2 (intensified/additional prevention goals) according to the risk stratification?
In DM patient with risk features (long standing DM and HT): aim for LDLC <1.8
What are the initial prevention goals and additional prevention goals in T2DM (well controlled DM, without established ASCVD or severe TOD, with estasblished ASCVD and/or severe TOD)?
How to assess the risk severity of patients with CKD without diabetes/ASCVD?
Familial hypercholesterolemia?
What is the prevention goals and additional prevention goals for patient with CKD and patients with FH for improving medical outcome?
What is the management for patients with established ASCVD (atherosclerotic cardiovascular disease) for step 1 and step 2?
What is the ESC/EAS guidelines for treatment of pharmacological LDL-C lowering?
If requires pharmacological management
High intensity statin first –> add ezetimibe (GLP1r agonist) if LDL-C goal not reacted –> then add PCSK9 inhibitor (evolumumab) which used as secondary prevention for very high risk patients and primary prevention (patients with FH and another major risk factor)
Who is screened for systematic CVD risk assessment?
