38.1 Cardiovascular Medicine I: Hypertension and Secondary Causes, Dyslipidemia, Stable Angina and Acute Coronary Syndromes, Post-MI Complications, Heart Failure and Shock Syndromes

Why this area matters

Heart disease is the leading cause of death in the Philippines, and hypertension is the most common chronic condition seen in primary care. The PLE asks you to recognize ACS on an ECG, choose reperfusion, start guideline-directed therapy for heart failure and resuscitate shock. Drug details are in the cardiovascular pharmacology sections; this section focuses on diagnosis and clinical decisions.

Hypertension

• Diagnosis:
  • use repeated, properly measured office readings (seated, correct cuff size, two readings) confirmed by home or ambulatory BP monitoring where possible;
  • hypertension is 140/90 mmHg or more by Philippine, ESH and WHO thresholds; the ACC/AHA 2017 threshold is 130/80 mmHg;
  • white-coat hypertension is high in the clinic but normal at home; masked hypertension is the reverse.
• Evaluation:
  • target-organ damage: left ventricular hypertrophy (ECG, echo), retinopathy, albuminuria and reduced eGFR, and prior stroke or CAD;
  • baseline tests: creatinine and eGFR, electrolytes, fasting glucose or HbA1c, lipids, urinalysis with albumin-to-creatinine ratio, and ECG;
  • total cardiovascular risk guides treatment intensity.
• Treatment:
  • lifestyle: salt below 5 g a day, weight loss, the DASH diet, exercise, limiting alcohol and stopping smoking;
  • drugs for stage 2 hypertension, or for stage 1 with high risk or organ damage;
  • most patients need two drugs, ideally in a single pill;
  • targets below 130/80 mmHg for most patients who tolerate them.
• Secondary hypertension: suspect it with onset before 30 years, resistant hypertension (uncontrolled on three drugs including a diuretic), sudden worsening, or suggestive features:
  • primary aldosteronism: hypertension with hypokalemia (often normal potassium); screen with the aldosterone-renin ratio;
  • renal artery stenosis: atherosclerotic in older smokers, fibromuscular dysplasia in young women; abdominal bruit, flash pulmonary edema, or creatinine rising more than 30% after an ACE inhibitor;
  • chronic kidney disease and glomerulonephritis;
  • pheochromocytoma: paroxysms of headache, sweating and palpitations;
  • Cushing syndrome, hyperthyroidism and obstructive sleep apnea (snoring, obesity, daytime sleepiness);
  • coarctation of the aorta: arm-leg BP difference and radiofemoral delay;
  • drugs: NSAIDs, oral contraceptives, steroids, decongestants and stimulants.
• Hypertensive emergency (severe hypertension with acute organ damage) needs IV drugs and controlled lowering. Urgency without organ damage is managed with oral drugs.

Dyslipidemia and cardiovascular risk

• Screening with a lipid profile in adults, earlier with diabetes, family history or other risk factors.
• Secondary causes: diabetes, hypothyroidism, nephrotic syndrome, cholestasis, alcohol and drugs (steroids, thiazides, antiretrovirals).
• Familial hypercholesterolemia: LDL of 190 mg/dL or more, tendon xanthomas, corneal arcus before 45, and premature CAD in the family.
• LDL targets by risk (ESC/EAS 2019):
  • very high risk (established ASCVD, diabetes with organ damage, severe CKD): LDL below 55 mg/dL and a 50% reduction;
  • high risk: below 70 mg/dL;
  • moderate risk: below 100 mg/dL.
• Treatment: lifestyle and statins first; add ezetimibe, then a PCSK9 inhibitor if targets are not met.
• Triglycerides above about 500 mg/dL (especially above 1,000) risk acute pancreatitis: treat with fibrates, diet, alcohol avoidance and glucose control.

Stable coronary artery disease

• Typical angina: constricting chest discomfort brought on by exertion or stress and relieved within minutes by rest or nitroglycerin.
• Tests:
  • resting ECG and echo;
  • coronary CT angiography or stress testing (exercise ECG, stress echo or perfusion scan) depending on likelihood;
  • invasive angiography for high-risk findings or refractory symptoms.
• Treatment:
  • aspirin (or clopidogrel) and a high-intensity statin for all;
  • beta-blockers or calcium channel blockers for symptoms, with sublingual nitroglycerin;
  • control of BP, diabetes and smoking;
  • revascularization (PCI or CABG) for refractory angina or high-risk anatomy (left main, three-vessel disease with diabetes or reduced EF).

Acute Coronary Syndromes (ACS)

Acute coronary syndromes encompass a spectrum of myocardial ischemia triggered by atherosclerotic plaque disruption, platelet activation, and coronary arterial thrombosis. ACS is categorized into ST-Elevation Myocardial Infarction (STEMI), Non-ST-Elevation Myocardial Infarction (NSTEMI), and Unstable Angina (UA) based on electrocardiographic (ECG) patterns and serum cardiac biomarkers.

Spectrum and Pathophysiology

• STEMI: Represents acute, transmural myocardial ischemia caused by complete thrombotic occlusion of an epicardial coronary artery. It presents with persistent chest discomfort and new ST-segment elevations (or new left bundle branch block with concordant ST changes) and elevated cardiac biomarkers.
• NSTEMI: Results from non-occlusive, subtotal thrombosis or dynamic vasospasm causing subendocardial necrosis. ECG reveals ST-segment depressions, T-wave inversions, or transient non-specific changes with elevated cardiac troponins.
• Unstable Angina (UA): Characterized by myocardial ischemia without detectable myocyte necrosis (normal troponin levels). Symptoms occur at rest, represent new-onset severe angina, or demonstrate a crescendo pattern.

ECG Localization and Culprit Vessels

Electrocardiographic ST elevation in contiguous leads localizes the ischemic territory and identifies the culprit coronary artery:

Biomarker Kinetics

• High-Sensitivity Cardiac Troponin (hs-cTnI and hs-cTnT): Preferred diagnostic biomarkers due to near-absolute myocardial tissue specificity. Troponins rise within 2 to 4 hours of onset, peak at 24 to 48 hours, and remain elevated for 10 to 14 days.
• CK-MB: Rises within 4 to 6 hours, peaks at 18 to 24 hours, and returns to baseline within 48 to 72 hours. It is clinically valuable for detecting early recurrent infarction (reinfarction) during the subacute phase.

Reperfusion Strategies and Emergency Pharmacotherapy

Time to myocardial reperfusion directly dictates myocardial salvage and survival:

1. Primary Percutaneous Coronary Intervention (PCI): The gold standard for acute STEMI. Primary PCI is recommended when the procedure can be performed within a door-to-balloon time of $\le 90\text{ minutes}$ at a PCI-capable hospital, or within $\le 120\text{ minutes}$ of first medical contact if inter-hospital transfer is required.
2. Fibrinolytic Therapy: Indicated for acute STEMI presenting within 12 hours of symptom onset when anticipated primary PCI-related delay exceeds 120 minutes. The target door-to-needle time is $\le 30\text{ minutes}$ using fibrin-specific agents (tenecteplase, alteplase, or reteplase). Absolute contraindications include prior intracranial hemorrhage, known cerebrovascular structural lesion, ischemic stroke within 3 months (except within 4.5 hours), active internal bleeding, or suspected aortic dissection.
3. Adjunctive Medical Regimen:
   • Dual Antiplatelet Therapy (DAPT): Aspirin ($162\text{ to }325\text{ mg}$ loading dose, followed by $81\text{ mg}$ daily indefinitely) plus a potent oral $P2Y_{12}$ inhibitor (Ticagrelor $180\text{ mg}$ load or Prasugrel $60\text{ mg}$ load; Clopidogrel $600\text{ mg}$ load before primary PCI when potent agents cannot be used; with fibrinolysis, Clopidogrel $300\text{ mg}$ load, or $75\text{ mg}$ without a load in patients older than 75 years).
   • Anticoagulation: Intravenous unfractionated heparin (UFH), enoxaparin, or bivalirudin.
   • Anti-ischemic Therapy: Sublingual or intravenous nitroglycerin (avoid if systolic blood pressure $< 90\text{ mmHg}$, heart rate $< 50\text{ bpm}$ or $> 100\text{ bpm}$, right ventricular infarction, or recent phosphodiesterase-5 inhibitor use). Oral beta-blockers (metoprolol tartrate or carvedilol) should be initiated within 24 hours in hemodynamically stable patients without signs of acute heart failure or cardiogenic shock.
   • High-Intensity Statin Therapy: Atorvastatin $80\text{ mg}$ or Rosuvastatin $40\text{ mg}$ daily started immediately regardless of baseline lipid levels.

Complications after myocardial infarction

• Cardiogenic shock after MI is treated with urgent revascularization, inotropes and vasopressors, and mechanical support.
• Secondary prevention after MI: aspirin plus a P2Y12 inhibitor for 12 months, high-intensity statin, beta-blocker, ACE inhibitor (especially with reduced EF), cardiac rehabilitation and stopping smoking.

Heart failure

• Common causes in the Philippines: hypertension, ischemic heart disease, rheumatic valve disease, cardiomyopathies (dilated, including alcoholic and peripartum) and thyroid disease.
• Clinical diagnosis: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, edema, raised JVP, an S3, crackles and hepatomegaly (the Framingham criteria combine these).
• Tests:
  • natriuretic peptides: BNP below 100 pg/mL or NT-proBNP below 300 pg/mL makes acute HF unlikely;
  • echocardiography gives the EF and the cause;
  • chest X-ray shows cardiomegaly, upper-lobe diversion, Kerley B lines and effusions.
• Precipitants of decompensation: non-adherence to drugs or salt restriction, ischemia, arrhythmias (especially atrial fibrillation), infection, uncontrolled hypertension, NSAIDs, anemia, thyroid disease and pregnancy.

Heart Failure (HF): Chronic GDMT & Acute Hemodynamics

Heart failure is a complex clinical syndrome resulting from structural or functional ventricular impairment, categorized by left ventricular ejection fraction (LVEF):

• HFrEF (Reduced Ejection Fraction): $\text{LVEF} \le 40\%$.
• HFmrEF (Mildly Reduced Ejection Fraction): $\text{LVEF } 41-49\%$.
• HFpEF (Preserved Ejection Fraction): $\text{LVEF} \ge 50\%$.

NYHA Functional Classification

• Class I: Cardiac disease without resulting limitation of ordinary physical activity.
• Class II: Slight limitation; comfortable at rest, but ordinary physical activity causes fatigue, palpitations, or dyspnea.
• Class III: Marked limitation; comfortable at rest, but less than ordinary activity causes fatigue or dyspnea.
• Class IV: Inability to carry on any physical activity without discomfort; symptoms present at rest.

The Four Pillars of Guideline-Directed Medical Therapy (GDMT) for HFrEF

In all patients with symptomatic HFrEF, four pharmacologic drug classes provide additive mortality reduction and must be titrated to maximum tolerated target doses:

1. Angiotensin Receptor-Neprilysin Inhibitor (ARNI): Sacubitril/valsartan is preferred over ACE inhibitors or ARBs. Sacubitril inhibits neprilysin (preventing breakdown of endogenous natriuretic peptides, bradykinin, and adrenomedullin), while valsartan blocks angiotensin II type 1 receptors. If switching from an ACE inhibitor to an ARNI, a mandatory 36-hour washout period is required to prevent life-threatening angioedema.
2. Evidence-Based Beta-Blockers: Specifically Carvedilol, Metoprolol Succinate (extended-release), or Bisoprolol. Beta-blockers must be initiated when the patient is euvolemic and hemodynamically stable, beginning at low doses and uptitrated every 2 to 4 weeks.
3. Mineralocorticoid Receptor Antagonists (MRAs): Spironolactone or eplerenone, indicated for NYHA Class II-IV with $\text{LVEF} \le 35\%$, provided serum potassium is $< 5.0\text{ mEq/L}$ and estimated GFR is $> 30\text{ mL/min/1.73 m}^2$.
4. Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors: Dapagliflozin ($10\text{ mg}$ daily) or Empagliflozin ($10\text{ mg}$ daily) reduce cardiovascular death and heart failure hospitalizations regardless of diabetes status.

Symptom Management: Loop diuretics (furosemide, bumetanide, torsemide) relieve pulmonary and peripheral congestion but do not confer independent survival benefits.

Acute Decompensated Heart Failure (ADHF): Forrester Hemodynamic Subsets

Acute heart failure decompensation is stratified based on clinical perfusion ("warm" versus "cold", cardiac index cutoff $2.2\text{ L/min/m}^2$) and pulmonary congestion ("dry" versus "wet", pulmonary capillary wedge pressure cutoff $18\text{ mmHg}$):

More on heart failure:

• HFpEF is treated with diuretics for congestion, an SGLT2 inhibitor, and control of BP, AF and comorbidities.
• Devices:
  • an ICD for EF of 35% or less with NYHA class II to III despite at least 3 months of therapy;
  • cardiac resynchronization therapy for EF of 35% or less with LBBB and QRS 150 ms or more.
• Self-care: daily weights, salt restriction, fluid limits in severe HF, vaccination and exercise training.

Shock syndromes

• Sepsis (Sepsis-3): life-threatening organ dysfunction from a dysregulated response to infection, with an acute rise in the SOFA score of 2 or more. qSOFA (RR 22 or more, altered mentation, systolic BP 100 or less) flags risk but is not used alone for screening.
• Septic shock: sepsis needing vasopressors to keep MAP at 65 mmHg or more with lactate above 2 mmol/L despite adequate fluids.
• Surviving Sepsis Campaign 2021 first-hour management:
  • blood cultures, then broad-spectrum antibiotics within 1 hour for possible septic shock or probable sepsis;
  • measure lactate and repeat it if raised;
  • 30 mL/kg of crystalloid (balanced solutions preferred) within the first 3 hours for hypotension or lactate of 4 mmol/L or more;
  • norepinephrine first-line to keep MAP at 65 mmHg or more, adding vasopressin and then hydrocortisone if needed;
  • source control (drain abscesses, remove infected lines).
• Anaphylaxis: IM epinephrine 0.5 mg (0.01 mg/kg) into the anterolateral thigh, repeated every 5 to 15 minutes, with fluids, oxygen, then antihistamines and steroids as adjuncts.
• Cardiogenic shock: treat the cause (revascularize an MI), give inotropes such as dobutamine with norepinephrine for hypotension, and use mechanical support in selected patients.