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The Nutrition Prevention and Reversal of Cardiovascular Disease: Fact or Fiction?

The Nutrition Prevention and Reversal of Cardiovascular Disease: Fact or Fiction?. Caldwell B. Esselstyn, Jr., MD. Highlights. The world’s advanced countries have easy access to plentiful high fat food; ironically, it is this rich diet that produces atherosclerosis

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The Nutrition Prevention and Reversal of Cardiovascular Disease: Fact or Fiction?

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  1. The Nutrition Prevention and Reversal of Cardiovascular Disease: Fact or Fiction? Caldwell B. Esselstyn, Jr., MD

  2. Highlights • The world’s advanced countries have easy access to plentiful high fat food; ironically, it is this rich diet that produces atherosclerosis • In the world’s poorer nations, many people subsist on a primarily plant-based diet, which is far healthier, especially in terms of heart disease • The time is long overdue to offer cardiovascular disease patients treatment for the causation of their disease • The present standard cardiology approach cannot cure patients, nor halt disease development, and is financially unsustainable

  3. Highlights • All patients in a non-emergency situation should be offered the option of plant-based nutrition to halt and reverse their disease by practitioners who are knowledgeable with this approach • Nutritional intervention, as shown in our study and others, has halted and even reversed CAD • The safety, diminished expense, and prompt, powerful, and persistent results in treating the cause of vascular disease by whole-food plant-based nutrition offer a paradigm shift from existing practice • Arrest and Reversal outcomes with Diet - No mortality - No morbidity - Benefits improve with time

  4. Update on PCSK9 Inhibitors and New Therapies Evan A. Stein, MD

  5. Highlights • Elevated low-density lipoprotein cholesterol (LDLC) levels in the plasma is the most important causative factor of atherosclerosis and associated ischemic cardiovascular diseases • The LDL receptor (LDLR) is the preferential pathway through which LDLs are cleared from the circulation • LDLs bound to the LDLR are internalized into clathrin-coated pits and subsequently undergo lysosomal degradation, whereas the LDLR is recycled back to the plasma membrane • Circulating PCSK9 binds the LDLR on the cell surface and is subsequently cointernalized together with the LDLR • This promotes the degradation of the receptor in the lysosome, rather than recycling to the plasma membrane. PCSK9 can also bind the LDLR intracellularly

  6. Highlights • By virtue of its role as a major inhibitor of the LDLR, PCSK9 has emerged as a hot new drug target to treat hypercholesterolemia and coronary heart disease • ODYSSEY, OSLER 1 & 2 trials have demonstrated that alirocumab and evolucumab decrease LDL by ~60% and CVD events by ~50% at 12-18 months • PCSK9 is a promising option for patients truly statin intolerant (or who don’t have adequate LDL lowering despite statin therapy) • But long term safety is still unknown and final CVD outcomes data pending

  7. New Treatments for Hypercholesterolemia: Apheresis, Mipomersen, Lomitapide & PCSK9 Inhibitors James M Falco

  8. Highlights • Apheresis has an important role in the management of two common complex lipid disorders associated with a high risk of premature atherosclerotic disease, familial hypercholesterolemia (FH) and Lp(a) hyperlipidemia • LDL apheresis is indicated in patients with LDL > 200 mg/dl with CHD, asymptomatic patients with LDL >300 mg/dl and in selected CHD patients with LDL >130 mg/dl with Lp(a) > 50-60 mg/dl • Studies have shown significant reductions of CV event stabilization and/or improvement of lesions and overall CV survival

  9. Highlights • Mipomersen is a second generation antisense oligonucleotide that targets apolipoprotein B • Mipomersen reduces all apolipoprotein B containing atherogenic particles and displays dose dependent reductions between 50-400 mg/week both as a single agent and in the presence of maximal lipid lowering therapy • Mipomersen is rapidly and extensively absorbed after subcutaneous administration and has an elimination half-life of approximately 30 days across species • No drug-drug interactions have been identified with Mipomersen

  10. Highlights • Lomitapideis a microsomal transfer protein inhibitor indicated as an adjunct to low fat diet and other lipid lowering therapies • It reduces LDL, total cholesterol, apo B and HDl cholesterol in patients with homozygous familial hypercholesterolemia (HoFH) • Inhibitors of proproteinconvertasesubtilisinkexin type 9 (PCSK9) represent a new therapeutic category of drugs for the treatment of dyslipidemia and atherosclerotic cardiovascular disease • Drugs which negate the action of PCSK9 can produce substantial reductions in atherogenic lipoprotein cholesterol-carrying particles and thereby hold the potential for further reducing events associated with atherosclerotic cardiovascular disease

  11. Statin Intolerance: Statin Side-Effects? Lisa Tannock, MD

  12. Highlights • In clinical practice 10-25% of patients report statin associated muscle symptoms (SAMS) or intolerance like Myalgia, myopathy and rhabdomyolysis • Patient related factors that can increase the risk of statin induced myopathy include: increasing age, female sex, renal insufficiency, hepatic dysfunction, hypothyroidism, diet (i.e grapefruit juice) and polypharmacy • The properties of statins that can increase the risk of statin induced myopathy include: high systemic exposure, lipophilicity, high bioavailability, limited protein binding, potential for drug-drug interactions metabolized by CYP pathways (particularly CYP450 3A4)

  13. Highlights • Statins may decrease LFTs that are high due to fatty liver. • If AST/ALT < 3 times ULN, it is ok to continue statin therapy • If muscle symptoms occur, measure CK and TSH • CK >10 x ULN: discontinue all lipid meals. CK <10 x ULN: measure weekly, if it is increasing discontinue medicines and if decreasing ok to continue statins • In case of SAMS, European Atherosclerosis Society (EAS) recommends to • Discontinue the statin and then retry • Try at least 3 different statins • Use maximum tolerated statin dose combined with non-statin lipid therapies

  14. Advanced Lipid Testing: LDL Particles for the Clinicians Peter Jones

  15. Highlights • Advanced lipid testing consisting of biomarkers which are lipid or non-lipid parameters beyond those included in a routine lipid profile enables clinicians to effectively measure and treat lipid abnormalities. • Biomarkers can be useful in determining disease state, rate and trait and helps to assess the initial ASCVD risk, before starting lipid-altering therapy but also to monitor the progress of therapy • Following tests which can be useful for assessing baseline risk and for on-treatment decisions • Evolved LDL cholesterol testing consisting of non-HDL, apoprotein B, LDL-P • Evolved HDL cholesterol testing consisting of HDL-P, apoprotein A1 • Lipoprotein (a)

  16. Highlights • Basic lipid panel (preferably fasting), with LDL and non HDL is required. A nonfasting non-HDL cholesterol still be useful • Further measures of atherogenic particle number (apo B, LDP-P) are not necessary since non-HDL is equivalent and sufficient even in discordant situations • Routine measurement of Lp(a) is not needed. It can be done for patients with a personal history of premature CVD, a family history of premature CVD, or familial hypercholesterolemia. • A high risk level for Lp(a) is >50 mg/dl • Lipid particle size and/or density is not helpful if the overall particle number is known

  17. Triglyceride Lowering Agents: Should they be used outside Lipid clinic? Eliot Brinton

  18. Highlights • Mendelian randomization data strongly suggest that hypertriglyceridemia (HTG) causes atherosclerotic cardiovascular disease (ASCVD) • Hence, triglyceride (TG) lowering treatment in HTG is now more strongly recommended to address the residual ASCVD risk than has been the case in earlier published guidelines • Fasting TG measurement is standard. Non-fasting TG predicts CVD risk in populations but is too variable in individuals • If non-fasting TG <200 mg/dl, fasting TG is not necessary. Remnant particle testing is controversial

  19. Highlights • Statins are the best-established agents for ASCVD prevention, and so are usually used as first-line treatment of TG levels less than 500 mg/dL • Statin monotherapy may fail to normalize high triglycerides and low high-density lipoprotein cholesterol, and it prevents only a minority of CVD events • Fibrates are the best-established agents for TG level lowering and are generally used as first-line treatment of TG levels greater than 500 mg/dL

  20. Highlights • Further treatment of lipid disorders that remain after statin monotherapy should help reduce the residual CVD risk • Fibrate monotherapy lowers high triglyceride levels, raises low high-density lipoprotein cholesterol, and reduces CVD risk • Hence, fibrates are recommended as an adjunct to statins for treatment of residual dyslipidemia and residual CVD risk

  21. Metformin: The Role of Its Non-Glycemic Effects in Cardiovascular Risk Reduction John Miles, MD

  22. Highlights • Metformin has proven itself as a front runner in the therapeutic armamentarium of type 2 diabetes and various other metabolic diseases • Metformin exerts most varied effects on both large and small vessels, as well as on haemostatic parameters • Metformin has remarkable and partly unique properties in the microcirculation, which can largely explain its long-term superiority in the UKPDS trial

  23. Highlights • Metformin has been associated with less CV morbidity and mortality, at least in part independently of improvement in glycaemic control and other risk factors, such as hypertension, obesity and dyslipidaemia • Metformin use has been associated with reduced mortality in patients with diabetes and heart failure • Metformin has demonstrated beneficial effects on systolic BP, heart rate, LV mass, stroke volume, cardiac index and cardiac work

  24. Dual-acting Saroglitazar effective for diabetic dyslipidemia with fewer side effects

  25. Highlights • In a 9-month, postmarketing study among Indians, Saroglitazar was well tolerated and effective in diabetes patients whose dyslipidemia was not controlled by statins • The 9-month study included 787 patients in India with diabetic dyslipidemia treated with 4 mg daily of Saroglitazar • Glycemic parameters were evaluated at baseline and at 3 months, 6 months, and 9 months. At 9-month follow-up: - Triglyceride levels were reduced by 43.8% - LDL cholesterol was reduced by 18.5% - Total cholesterol was reduced by 23.1%

  26. Highlights • A significant improvement was seen in HDL cholesterol, which rose from 41.0 ± 14.73 mg/ dL at baseline to 44.5 ± 8.31 mg/dL • HbA1C dropped from 8.5 ± 1.37% to 7.0 ± 0.78% at 9-month follow-up (P<0.0001), and fasting and postprandial blood sugar were also significantly reduced at 9-month follow-up by 28.1% and 35.2% (P<0.0001) respectively • Treatment with the drug was not found to be associated with an increase in body weight (73.9 ± 11.92 kg at baseline to 72.4 ± 11.55 kg at 9-month follow-up) and there were no reports of serious adverse events among users

  27. Insulin pump therapy superior to multiple daily injections for HbA1c levels

  28. Highlights • Lee and colleagues conducted a run-in period for the OpT2mise trial for dose optimization on 495 individuals with poor glycemic control on multiple daily injections • Following the run-in phase, 331 participants with HbA1c levels of 8% to 12% either continued multiple daily injections (n = 163) or switched to pump therapy (n = 168) for 6 months to compare the two treatment types • After 6 months, HbA1c levels decreased by 1.1% in the pump therapy group and by 0.4% in the multiple daily injections group (P < .001) • Compared with participants in the injections group, participants in the pump therapy group were more likely to achieve HbA1c levels below 8% (P < .001)

  29. Highlights • Total daily insulin doses were greater in the injections group (122 U) compared with the pump therapy group (97 U) after 6 months (P < .0001) • The pump therapy group had significantly lower 24-hour sensor glucose values at 6 months compared with the injections group (P < .05) after comparing results to the first CGM study • The pump therapy group also spent fewer minutes per day in hyperglycemia compared with the injections group (P < .001) • Improved treatment satisfaction was significantly associated with greater HbA1c reductions at 6 months for the pump therapy group but not the injections group (P < .05)

  30. Analysing Endothelial Dysfunction In Type2 Diabetes Mellitus Patients Using Flow Mediated Dilatation Score

  31. Highlights • A study was performed to determine early stage CVD risk in type 2 DM patient using FMD (flow mediated dilatation) score – correlating it with acceleration of inflammatory process of vascular injury. • A total of 50 (36 F and 14 M) patients with type 2 DM of more than 10 years with age above 50years were screened for FMD score along with 30 (17 F 13 M) healthy controls, using Angiodefender.

  32. Highlights • The FMD score in 50 type 2 DM patients showed that 70% (n=35) patients suffered from impaired endothelial function and increased arterial thickness; 16% (n=8) patients suffered from endothelial dysfunction, arterial stiffness and atherosclerosis whereas the remaining 14% had normal endothelial function. • On the other hand in the healthy counterparts, the FMD score was normal in 80% (n=24) patients. • Flow mediated dilatation score can be effectively used as a marker to determine the vascular injury and endothelial dysfunction in patients with type2 DM.

  33. Correlation of left ventricular hypertrophy & left ventricular diastolic dysfunction with HbA1c in newly diagnosed type 2 diabetics

  34. Highlights • This study was carried out to assess the frequency of left ventricular hypertrophy (LVH) and left ventricular diastolic dysfunction (LVDD) in normotensive newly diagnosed type 2 diabetic patients by using 2D echocardiography and correlation with HbA1C. • 100 newly diagnosed normotensive type 2 diabetes mellitus patients between 30 - 60 year of age were enrolled from endocrine OPD of a tertiary care center during a period of 1 year.

  35. Highlights • Results: 41 % patients had LVDD and 37 % patients had LVH. • The mean HbA1C of population with LVDD was 7.67 ± 0.90 % and that with LVH was 7.74 ± 0.91 %. The LVDD and LVH were positively correlated with HbA1C (p value = 0.0057 & p value = 0.0011) respectively • Left ventricular diastolic dysfunction & left ventricular hypertrophy were positively correlated with HbA1C in newly diagnosed T2DM population

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