9.1 MNT for Cardiovascular Disease, Hypertension, and Dyslipidemia

Cardiovascular diseases (CVD) remain the primary cause of morbidity and mortality in the Philippines and globally. Atherosclerotic cardiovascular disease (ASCVD), systemic arterial hypertension, and congestive heart failure share common pathophysiological roots governed by vascular endothelial dysfunction, chronic vascular inflammation, hemodynamic shearing forces, and atherogenic dyslipidemia. Evidence-based Medical Nutrition Therapy directly addresses these cellular and vascular mechanisms to retard disease progression, stabilize vulnerable plaques, and reduce fatal vascular events.

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Cellular Pathophysiology of Atherosclerosis

Atherosclerosis is not a simple degenerative disorder of passive lipid accumulation, but an active, chronic inflammatory process affecting large and medium-sized elastic and muscular arteries:

+-----------------------------------------------------------------------------------------+
|                         Atherosclerotic Inflammatory Cascade                            |
|                                                                                         |
|  [Endothelial Injury] -> [LDL Infiltration & Oxidation] -> [Macrophage Scavenger Uptake] |
|                                                                     |                   |
|  [Thrombotic Rupture] <- [Unstable Fibrous Cap] <- [Fatty Streak / Foam Cells] <--------+ |
+-----------------------------------------------------------------------------------------+

1. Endothelial Dysfunction: Chronic insults—including elevated oxidized low-density lipoproteins (oxLDL), cigarette smoking toxins, sustained shear stress from arterial hypertension, advanced glycation end-products (AGEs) in diabetes, and hyperhomocysteinemia—impair endothelial nitric oxide (NO) bioavailability. The endothelium expresses cellular adhesion molecules: Vascular Cell Adhesion Molecule-1 (VCAM-1) and Intercellular Adhesion Molecule-1 (ICAM-1).
2. Lipoprotein Infiltration and Retention: Circulating apolipoprotein B-100 (ApoB) containing lipoproteins, predominantly LDL and remnant particles, penetrate the compromised endothelial barrier and bind to subendothelial matrix proteoglycans in the arterial intima.
3. Lipid Oxidation: Trapped LDL undergoes oxidation by vascular reactive oxygen species (ROS) and enzymatic lipoxygenases, generating oxidized LDL (oxLDL). Oxidized LDL acts as a powerful local chemoattractant and cytotoxic agent, stimulating endothelial release of monocyte chemoattractant protein-1 (MCP-1) and macrophage colony-stimulating factor (M-CSF).
4. Foam Cell Formation: Circulating blood monocytes adhere to VCAM-1, migrate into the intima, and differentiate into active macrophages. Macrophages express scavenger receptors (SR-A, CD36) that engulf oxLDL via unregulated receptor-mediated pinocytosis. Unlike native LDL receptors, scavenger receptors lack negative feedback inhibition, allowing macrophages to become engorged with cholesteryl esters, transforming into lipid-laden foam cells.
5. Fatty Streak to Fibrous Plaque: Apoptosis of foam cells creates a necrotic lipid core surrounded by cellular debris. Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-$\beta$) released from platelets and macrophages induce vascular smooth muscle cells (VSMCs) to migrate from the media into the intima. VSMCs proliferate and secrete extensive collagen matrix, forming a protective fibrous cap over the necrotic lipid core.
6. Plaque Rupture and Acute Thrombosis: Macrophages secrete matrix metalloproteinases (MMPs), collagenases, and elastases that degrade interstitial collagen in the fibrous cap. Thinning of the cap makes it vulnerable to mechanical shear stress. Plaque rupture or endothelial erosion exposes highly thrombogenic subendothelial tissue factor and collagen to circulating platelets, activating the coagulation cascade and triggering acute intraluminal thrombus formation, culminating in acute myocardial infarction (AMI) or ischemic cerebrovascular accident (CVA).

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Dyslipidemia Classification and Medical Nutrition Therapy

Clinical lipid management adheres to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) Therapeutic Lifestyle Changes (TLC) diet and on Philippine clinical practice guidelines for dyslipidemia:

Standard Plasma Lipid Reference Cutoffs

In patients with established ASCVD or very high cardiovascular risk, the target LDL-C is $< 70\text{ mg/dL}$ ($1.8\text{ mmol/L}$) or $< 55\text{ mg/dL}$ ($1.4\text{ mmol/L}$).

The NCEP ATP III Therapeutic Lifestyle Changes (TLC) Diet

• Saturated Fatty Acids (SFA): $< 7\%$ of total daily calories. SFA (primarily palmitic $C16:0$, myristic $C14:0$, and lauric $C12:0$ acids) downregulate hepatic LDL receptor expression, reducing clearance of circulating LDL. Replace SFA with cis-monounsaturated fatty acids (oleic acid $C18:1$) and polyunsaturated fatty acids (linoleic acid $C18:2$).
• Trans-Fatty Acids: Complete elimination ($< 1\%$ or $0\text{ g}$). Industrial trans fats (partially hydrogenated vegetable oils) increase LDL-C, suppress HDL-C, and elevate systemic vascular inflammation.
• Dietary Cholesterol: $< 200\text{ mg/day}$.
• Total Fat: 25% to 35% of total daily energy.
• Soluble Viscous Fiber: $10 - 25\text{ g/day}$ (within a total dietary fiber intake of 25 to 35 g/day). Soluble viscous fiber fractions (beta-glucan from oats and barley, psyllium seed husk, pectin from fruits, guar gum from legumes) bind bile acids in the intestinal lumen, accelerating their fecal excretion. This interrupts enterohepatic recirculation, forcing the liver to convert endogenous hepatic cholesterol into new bile acids, thereby upregulating hepatic LDL receptors and lowering circulating LDL-C by 5% to 10%.
• Plant Stanols / Sterols (Phytosterols): $2\text{ g/day}$ (consumed as fortified spreads or capsules). Plant sterols possess a chemical structure nearly identical to cholesterol, competitively displacing dietary and biliary cholesterol from intestinal mixed micelles. Unabsorbed cholesterol is excreted in the feces, reducing serum LDL-C by 6% to 15% without lowering protective HDL-C.
• Hypertriglyceridemia Management: For serum triglycerides $> 150\text{ mg/dL}$ (and especially $> 500\text{ mg/dL}$ where acute pancreatitis risk is elevated): completely eliminate alcohol; severely restrict added refined sugars, sucrose, and high-fructose corn syrup (HFCS accelerates hepatic lipogenesis); limit refined starches; reduce total dietary fat; promote weight reduction; and supplement therapeutic marine omega-3 fatty acids ($2 - 4\text{ g/day}$ of EPA + DHA), which suppress hepatic VLDL synthesis and accelerate chylomicron clearance via lipoprotein lipase activation.

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Systemic Hypertension and the DASH Eating Plan

Blood Pressure Classification (2017 ACC/AHA)

WHO (2021) and the European Society of Hypertension still define hypertension as a blood pressure of 140/90 mmHg or higher, so read which classification a question names.

Dietary Sodium Standards and Salt Equivalencies

Sodium is the primary cation of the extracellular fluid, regulating osmotic pressure and intravascular volume. In salt-sensitive hypertension, excess sodium intake expands plasma volume and elevates peripheral vascular resistance.

• Standard Dietary Restriction: $< 2{,}300\text{ mg sodium/day}$ (approx. $100\text{ mmol}$ or 1 level teaspoon of table salt).
• Strict / Optimal Restriction: $< 1{,}500\text{ mg sodium/day}$ (approx. $65\text{ mmol}$), recommended for adults with established hypertension, diabetes, chronic kidney disease, or individuals $> 50\text{ years}$.
• Mathematical Salt Equivalency: Table salt (sodium chloride, $\text{NaCl}$) is 40% sodium and 60% chloride by molecular weight:

$1\text{ g NaCl} = 400\text{ mg Sodium} = 17.4\text{ mEq Sodium}$ $1\text{ level teaspoon of salt} \approx 5.8\text{ g NaCl} \approx 2{,}320\text{ mg Sodium}$

The DASH (Dietary Approaches to Stop Hypertension) Eating Plan

The DASH trial demonstrated that a diet rich in fruits, vegetables, whole grains, and low-fat dairy—providing generous amounts of potassium ($4{,}700\text{ mg/day}$), calcium ($1{,}240\text{ mg/day}$), magnesium ($500\text{ mg/day}$), and dietary fiber ($30\text{ g/day}$)—reduces systolic blood pressure by 8 to 14 mmHg in hypertensive patients:

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Congestive Heart Failure (HF) and Cardiac Cachexia

Heart failure is a complex clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection of blood:

• Compensated Heart Failure: The heart maintains adequate tissue perfusion through compensatory mechanisms (ventricular remodeling, myocardial hypertrophy, activation of the renin-angiotensin-aldosterone system [RAAS], and sympathetic nervous system discharge), without overt clinical pulmonary edema.
• Decompensated Heart Failure: Compensatory mechanisms fail, precipitating severe pulmonary and systemic venous congestion, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, hepatomegaly, ascites, and peripheral pitting edema.

Sodium and Fluid Restrictions in Heart Failure

• Sodium: Standard restriction is $2{,}000\text{ mg/day}$ (approx. $88\text{ mEq}$). Rigid restrictions ($< 1{,}000\text{ mg/day}$) are no longer advised because severe palatability impairment leads to malnutrition and may cause neurohormonal overactivation.
• Fluid: Restriction to $1.5 - 2.0\text{ L/day}$ is reserved for patients with decompensated heart failure, severe peripheral volume overload, refractory edema, or dilutional hyponatremia (serum sodium $< 130\text{ mEq/L}$).

Cardiac Cachexia: Pathophysiology and Nutritional Repletion

Cardiac cachexia is a severe, life-threatening complication occurring in up to 10% to 15% of advanced heart failure patients (NYHA Class III and IV):

• Diagnostic Definition: Unintentional, non-edematous weight loss of $> 5\%$ of baseline body weight over 6 to 12 months, accompanied by severe depletion of skeletal muscle (sarcopenia), adipose tissue, and somatic bone mineral density.
• Etiology: Driven by a chronic neuroendocrine and hyperinflammatory storm. Elevated circulating pro-inflammatory cytokines—Tumor Necrosis Factor-alpha (TNF-$\alpha$, historically termed cachectin), Interleukin-1 (IL-1), and Interleukin-6 (IL-6)—drive severe hypermetabolism, cellular proteolysis, and anorexia. Concurrently, right-sided ventricular failure causes splanchnic venous congestion, inducing gut mucosal edema, which produces early satiety, postprandial nausea, and cellular malabsorption of nutrients.
• Nutritional Prescription:
  • Energy: $30 - 35\text{ kcal/kg/day}$ (based on dry, edema-free body weight) to meet elevated resting energy expenditure; can increase up to $40\text{ kcal/kg/day}$ during active repletion.
  • Protein: $1.2 - 1.5\text{ g/kg/day}$ dry weight to restore negative nitrogen balance and preserve diaphragmatic and skeletal muscle mass.
  • Meal Pattern: Small, frequent, calorie-dense feedings (6 meals/day) to prevent diaphragmatic elevation, reduce abdominal pressure, and avoid postprandial splanchnic blood pooling that precipitates hypotension and angina.

Critical Pharmacological and Micronutrient Interactions

• Loop Diuretics (Furosemide, Bumetanide, Torsemide): Inhibit the $\text{Na}^+-\text{K}^+-2\text{Cl}^-$ symporter in the thick ascending limb of the loop of Henle. Chronic aggressive administration accelerates profound urinary wasting of potassium, magnesium, and thiamin (Vitamin $B_1$).

• Potassium-Sparing Diuretics (Spironolactone, Eplerenone) & ACE Inhibitors: Inhibit aldosterone receptors or angiotensin-converting enzyme, leading to potassium retention. Patients must avoid salt substitutes composed of potassium chloride (KCl) and monitor dietary potassium intake to prevent lethal cardiac hyperkalemia ($> 5.5\text{ mEq/L}$).