CAD

Cardiac Anatomy

Coronary Arteries

Athlerosclerosis

Athlerosclerosis occluds arteries, and when a large amount of a coronary artery is obstructed, angina can occur. The process of athlerosclerotic development is as follows:

  1. LDL accumulation and oxidation in the wall of a vessel
  2. Macrophage infiltration and uptake of the LDL deposit
  3. Formation of foam cells
  4. Smooth Muscle proliferation and Cap formation
  5. Cap rupture
  6. Thrombosis

General Angina

Pathophysiology

Oxygen demand to cardiac tissue exceeds the ability of coronary circulation to supply oxygen to the cardiac myocytes, leading to ischemia and chest pain

Oxygen Supply and Demand

Preload: Decreased preload is caused by veinous vasodilation, resulting in decreased oxygen consumption and increased myocardial perfusion

Afterload: Decreased afterload is caused by arterial vasodilation, leading to decreased oxygen consumption

Heart Rate: Decreased HR leads to decreased oxygen consumption and increased coronary perfusion

Risk Factors

Stable Angina

Pathophysiology

Stable angina is a demand ischemia caused by a temporary increase in O2 demand by cardiac myocytes in the prescense of a diminished O2 supply, most commonly the result of severe ASCVD leading to significant decreases in blood flow (>70%) through the coronary arteries without myocardial necrosis. Stable angina can be of either a fixed threshold, a variable threshold, or both. Stable angina should have stable characteristics for at least 2 months.

Clinical Presentation and Dx

Dx

PQRST

Common Precipitating Factors

EKG Findings

ST-Depression only during episodes of angina, EKG is otherwise unremarkable

Treatment

Common Drug Classes for Treatment

Algorithm

SIHD Management Algorithm

Anti-Platelet Therapy

*following ACS only

Primary Prevention

Patients 50-69 with ≥ 10% 10-year CVD risk should be initiated on low-dose aspirin indefinitely if they have no additional bleeding risk. Older patients can continue ASA or initiate ASA; however, shorter life expectancy means the risks may outweigh the benefits. There is insufficient evidencefor a recomendation in patients under 50.

Secondary Prevention

Interventions Drugs Duration
SIHD ASA 81mg QD*^ Indefinitely
Elective PCI + BMS ASA 325mg before then 81mg QD & Clopidogrel 300-600mg before then 75mg QD ASA: Indefinitely; Clopidogrel: Minimum of 1mo, typically 12mo
Elective PCI + DES ASA 325mg before then 81mg QD & Clopidogrel 300-600mg before then 75mg QD ASA: Indefinitely; Clopidogrel: Minimum of 6mo, typically 12mo
PCI/Stent + CABG Restart regimine for stent ASA: Indefinitely; Repeat duration of stent (i.e. minimum set by kind of stent, 12mo typical)
CABG ASA 81mg QD & Clopidogrel 75mg QD ASA Indefinitely; Clopidogrel 12mo

*Pts with absolute contraindications or significant intolerance to ASA can initiate Clopidogrel 75mg QD

^DAPT: Dual Antiplatelet Therapy may be given despite lack of evidence in high risk patients

DAPT Score and Risk of DAPT Duration

Characteristic Points
Age ≥ 75 -2
Age [65,75) -1
Age < 65 0
Current Smoker 1
DM 1
MI at Presentation 1
Prior PCI or MI 1
Stent Diameter < 3mm 1
Paclitaxel-eluting Stent 1
CHF with LVEF < 30% 2
SVG PCI 2

Scores ≥ 2 favor prolonged therapy, while < 2 have an unfavorable benefit/risk ratio for prolonged therapy (use standard therapy).

ACEIs in CAD

ACEIs and ARBs have been show to stabilize plaques, improve endothelial function, inhibit smooth muscle migration, decrease macrophage infiltration, and possibly decrease oxidation of LDL. All CAD patients, especially those with CHF with LVEF ≤ 40%, HTN, DM, or CKD should be on an ACEI or ARB.

Symptomatic Control

Acute Nitrates

SL Nitroglycerin is the preferred agent for acute attacks, given as either 0.3-0.6mg SL tabs or 0.4mg/spray SL spray. NTG tablets cannot be stored in vials other than that which they are shipped in, and cannot, by law, have childproof caps. It is appropriate to have a patient keep a diary of nitrate use to record the frequency of their attacks the frequency of rescue NTG use.

Dosing

  1. Sit Down (Risk of Hypotension)
  2. Take 1 dose
  3. Wait 5 minutes
  4. If pain does not resolve, call 911 and take a second dose
  5. Take a maximum of 3 doses as needed

β-Blockers

Beta-Blockers work via decreasing myocardial contractility and heart rate, decreasing oxygen demand. Cardioselective agents such as Metoprolol (<100mg dose) and Atenolol (<50mg dose) are prefered, and beta-blocker with intrinsic sympathomimetic activity should be avoided due to the increased resting HR. β-blockers should be dosed to achieve either: RHR 50-60, exercise HR < 100, or exercise HR 75% of HR causing angina. For the specific behavor of β-blockers, see their section in Sympatholytics.

CCBs

Long acting DHP CCBs or non-DHP CCBs are appropriate therapy choices for prevention of anginal episodes. Consider the distinct behaviors of the DHP (vasodilatory similar to nitrates) and non-DHP (negative inotropes and chronotropes, similar to β-blockers, but with small amounts of vasodilation) classes in determining appropriate therapy. Non-DHPs have the significant and unique monitoring parameter of constipation, especially verapamil. IR DHP CCBs should be avoided due to marked tachycardia.

Chronic Nitrates

ISDN, ISMN, and transdermal NTG are commonly used. These agents should not be used as monotherapy due to a required washout period of 10-12hrs with no drug on board to prevent tolerance. Other downsides include frequency of administration (BID-QID).

Ranolazine

Ranolazine inhibits late-Na influx into cardiac myocytes, which during ischemia can change the sodium gradient enough to reverse Ca transport into the cell, creating a positive feedback loop of contraction and damaging the ischemic tissue. Ranolazine has no impact on BP or HR, but can cause long Q-T intervals, which has been shown to relate to increased risk of sudden cardiac death. Ranolazine is a third line agent and is typically used in combination with multiple other agents or if adequate control cannot be reached with dual therapy due to decreased HR and BP.

Side Effects

Ivabradine

Ivabradine can be used off label for angina in adults unable to tolerate β-blockers, with no arrhythmias and a RHR ≥ 70. This medication can also be used in combination with β-blockers if adequate control could not be reached with an adequate β-blocker dose.

Compelling Indications

Therapies to Avoid with Other Conditions

Prinzmetal’s (Variable) Angina

Pathophysiology

Prinzmetal’s angina is a supply ischemia resulting from spontaneous vasospasm in the coronary vessels, typically the result of athlerosclerotic insult to the endothelium, leading to a short-lived ischemia. Prinzmetal’s angina typically presents at night when parasympathetic tone is higher.

Treatment

Author: Corbin Cox
Created: 2018-1-29
Last Updated: 2018-2-21