Cardiovascular Diseases: Risk Factors and Prevention

Cardiovascular Diseases

• Leading cause of death globally

Risk Factors

• Non-modifiable: genetics, age, sex, ethnicity
• Modifiable: hypertension, diabetes, obesity, smoking, physical inactivity, dyslipidemia, excessive alcohol
• Female-specific: pregnancy, menopause, PCOS, inflammatory diseases, gestational diabetes, stress/depression

Cholesterol

• Lowering LDL cholesterol reduces cardiovascular disease risk
• Even small reductions benefit high-risk patients

Hypertension

• Increases atherosclerosis, heart failure, stroke, kidney failure risk
• Accounts for 62% of strokes and 49% of coronary artery diseases (CAD)
• Mortality risk increases with systolic BP ≥90mmHg and diastolic BP ≥75mmHg

Smoking

• Responsible for 50% of preventable deaths in smokers
• Increases cardiovascular risk 5-fold in smokers under 50, hazardous, even secondhand

Diabetes Mellitus

• Doubles cardiovascular risk, type 2 diabetes particularly risky for women
• Often associated with dyslipidemia and hypertension

Obesity

• BMI and waist circumference correlate with ASCVD and diabetes risk

Inflammation

• Proteins like CRP, cytokines (IL-1, IL-6 ), and biomarkers (selectin-P, CD40ligand, myeloperoxidase, plasma protein A, ST2, fibrinogen) predict cardiovascular risk, even with low LDL cholesterol

Lipid Metabolism & Atherosclerosis

• Lipids transported via lipoproteins are key in atherosclerosis

LDL

• ("bad" cholesterol) crosses arterial endothelium, promotes plaque formation

HDL

• ("good" cholesterol) removes cholesterol from arteries, reducing cardiovascular risk

Triglycerides

• Elevated levels increase cardiovascular risk, diet-dependent

Lipoprotein (a)

• Genetically determined, linked to higher cardiovascular disease risk
• Lipid & protein particle resembling LDL, with additional APOLIPOPROTEIN (a): apoB-100, apolipoprotein a, triglycerides, cholesterol, membrane phospholipids
• Only 20% of cholesterol intake is dietary, with apoB chylomicron transport, while 80% synthesized by the liver

Atherosclerosis

• Chronic, progressive condition of plaque formation, LDL-C crosses the endothelium, damaging it
• Monocytes phagocytize LDL, become FOAM CELLS, releasing ROS, and forming oxidized -> viscous cycle
• Plaques enlarge, reduce artery diameter, or rupture, causing thrombi -> which can completely block arteries causing infarction and stroke or emboli

Lipid Profile Measurement Recommendations

• Recommended for everyone, especially those at higher risk needing early evaluation

Risk Groups Categories

• Adults with family history of dyslipidemia may have genetic anomalies
• Young adults history of early cardiovascular disease: men <35 years and women <45 years with family cardiovascular events
• People with abdominal obesity: waist circumference >102 cm in men and >88 cm in women
• People with chronic conditions and increased CV risk

Chronic Kidney Disease (CKD)

• Alters lipid metabolism, accelerating atherosclerosis

Chronic Inflammatory Diseases. RA, Psoriasis etc: systemic inflammation

• Contributes to increased cardiovascular risk

Erectile Dysfunction

• Early sign of endothelial dysfunction and atherosclerosis

HIV Patients on Antiretroviral Therapy

• Antiretroviral drugs alter lipid metabolism, increasing cardiovascular risk
• Elderly (>75 years) with multiple cardiovascular risk factors: cardiovascular prevention remains a priority if life expectancy is good

Children At familial risk

• Family history of dyslipidemia with premature cardiovascular disease is a risk
• Overweight/obese children: fat accumulation leads to dyslipidemia, increasing early atherosclerosis risk

Apolipoprotein B (ApoB)

• Optimal marker
• Direct indicator total atherogenic in blood thus more accurate
• Has role in cardiovascular disease, better predictor than LDL-C
• Standardized, automated, economical, and accurate
• No fasting needed, chylomicrons transport less than 1% of particles ApoB
• Useful/ people with hypertriglyceridemia to family history of cardiovascular disease

Standard Lipid profile

• Total cholesterol
• HDL-C = good cholesterol
• Triglycerides =TG
• LDL-C calculate to TDTC---HDLC-TG/5 in mg/dL
• LDL- direct measurement but also estimated with Friedewald or greater but is not valid when triglycerides are greater then 400mg/dL

Traditional test or Fasting test?

• Traditionally fasting done prevent meals from affecting lipids.
• Without fasting triglicerides is 27 mg/dL increased not commiitingly evaluating risk in most cases
• For Very high triglicerides or high likely for familial hypertriglyceridemia

Dyslipidemia

• Divided in primitive.genetic then secondary

Heterozygous Familial Hypercholesterolemia

• Auto dominantly recessive mutation LDL >/ 190mg/dL
• Requires Family assessment.exam.bloodwork. LDL test

Polygenic Hypercholesterolemia

More common form from interactive envrionemtn reduced expression of LDL Chol \ increase in circle no tendencies.

Familial combined Hyperlipidemia

increase LDL of 160mg/dL then increases of 200 mg/dL, one familial

Familial HyperTriglyceridemia: High Epacto of reduced clearance can increase Risk for ischemic

Secondary Causes of Dyslipidemia

• Hypercholesterolemia--- hypo thyroidism
• Hypertriglyceridemia---Alchool
• Combined---nephritis of acromegaly.

Algorithmic Diagnosis

• Increase in cholesterol and triglycerides definition assessment evaluate family stratify.

Stratification of the Cardiovascualr Risk CV Risk

eval process of person develops cardio event in ten years helps to strategy patients treatment Cathegories Apperaing healthy

Modified Risk factors

stress and ethnicity inflammation all gender and sex factors.

4 Risk Categories

low moderate Alto all Ato Model

Score Score System: Evaulation

used to calculate geographical and age and arterial smoke cholesterol

Diabetes Mellitus

• The pancreas regulates blood sugar through insulin which lowers when glucose is high, with glucagon to increase and regulate blood glucose
• Insulin facilitates glucose storage in muscles/brain/fat tissue, liver glycogen synthesis, and reduces hunger
• Glucagon stimulates hepatic gluconeogenesis, raising blood sugar, however alters blood sugar levels to alter chronic hyperglycemia

Types of Diabetes Mellitus (DM)

• Type 1 DM: autoimmune disease destroying pancreatic beta cells, causing absolute insulin deficiency, insulin dependent, typically in childhood
• Type 2 DM: insulin resistance, reduced tissue response to insulin Initially, pancreas compensates, but beta cells decline over time, related to obesity, increases with age Diagnosis of DM: relies on parameters
• Fasting glucose ≥126 mg/dl
• 2-hour glucose post-OGTT ≥200 mg/dl
• Glycated hemoglobin (HbA1c) ≥6.5%

Evolution of Diabetes

• Reduced Glucose Tolerance (IGT), insulin resistance
• Increased Fasting Glucose (IFG): reduced insulin production
• A definite: chronic hyperglyceima

Symptoms

• Polyuria and nycturia due to glucose eliminated
• polydipsia
• dysuria
• reduced growth

Micro complications on short

damages small and big blood

• retinopathy is leding to blindness
• nerve damage
• heart disesae. Macro damages is arterials
• increase stroke

Hyperuricimia is meta

Lactic acid one prod of urine derives from acid and diets removed main by kidneys if concentrat is high

• saturations
• crystal

Gota is uncharachterized

• the increase and precip. in the tissus liquids organic art.
• increase productio to mix

Diagnosis

• measure to find diet isopurin and isocaloric = normals increased an dreduced levels

Natural story of Increase

• increased rate of gout pain
• chronical pain
• nepropathy Treatment of is acid decrease production like diet or alchohol or food

Metabolic and Obesity Syndromes

• Abdominal cirumference standing b/w iliac end
• increase weight leads to a problems growing
• multifactoial elements: genetic and environmental influence
• The caloric supereates then body will overdo
• With age the fat comes to stay sarcopeneic
• Reduction in fat but increase fat and disab
• Fat is in abdomen
• The main issue related to central.obse leads to : increase in lipid glucomea high BP mediators in. inflammation decreases adipo. can alter circ increased Meta

Hypertension

Categories

• Hypertension of first grade: systolic > 140 mmHg, diastolic > 90 mmHg
• Hypertension of second grade: systolic > 160 mmHg, diastolic > 100 mmHg
• Hypertension of third grade: systolic > 180 mmHg, diastolic > 110 mmHg

Epidemiology

• Affects 1 billion people worldwide and is a risk factor for various cardio event such as attack or heart or stroke
• By 2025 projected at 1.5 billion
• Underestimated by 62-49 in elevations
• After menopause prevalence shifts the impact on the population

Regulation

• Heart rate: power
• Peripheral

Vascular Regulation

• Vasocontritros: increasing
• Vasodoaltors: reduction
• Arterioles- vasocontrion and main targer for therapies.

Kidney is fundamentall

• Reining trasnfomrs and turns on with angio,
• Angiotensin provacs and increases sod.
• Natric peptides inhibit the reabsorb reduce and vasodialt

Classifcations Hypertension

• Essential, idiothatc origin can creaste alters and functiosn
• Secondary issues linked to kidney or cardiac

Diagnosis and Screening

• Collect and assses and and habits the
• test bloods

Organs damages.

• cns : issues cephalea
• lungs and dyspnea
• kindye and urinating

Level One Screening

• e c g , proteins EGFR, retinopathy

Two

• e cho #####Stratification of theRisk Therapeis depensn don and can do : change lyfesitle and necessary ####Modificatiosn ind pendant of med, do modificatiosn weight reductiion, dash Diet,

Pharmaco

increases rate and reduction of plasmic

Secondary hypertensionsions

resistant patients must look for some common traits .and causes

• apena or renal or endocrine

Apnea Sleep.

• closed airways with a disruption
• symtpos
• pollisotonography measure

Endocrine Secondary

altered regulation with multiple thryods diseases and causes

Surrenal with medullare is split in cortal

• tumors are cushing and primary also decrease sod.

4 Syndrom

High cortisol causes due to multiple conditions #####Clincial manifestos: full mson increase or ireegularites. diagnois cut off and what to eat cardiio inihibitors.

Complications Cardiaco is failures.

• cardio fails
• physiologica cycles
• diastople si empties to ventricels .

Explore cardiovascular diseases, the leading cause of death globally, and their risk factors, including genetics, hypertension, and diabetes. Learn how lowering LDL cholesterol and managing hypertension can reduce the risk of heart failure and stroke. Understand the impact of smoking and diabetes on cardiovascular health.