HOW TO TREAT 31
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HOW TO TREAT 31
Box 4. Issues to consider in refractory angina
• Has the patient developed obstructive CAD?
• Perform or repeat functional coronary angiography seeking confirmation of VSA that would benefit from a high dose CCB.
• Consider other antinociceptive and non-pharmacological treatments( MVA – external enhanced counterpulsation, coronary sinus reducer, antidepressants, methylxanthines, analgesics, transcutaneous electric nerve stimulator, spinal stimulators; VSA – stellate ganglion block, hormone therapy, analgaesics).
Source: Beltrame JF et al 2021 81
component to myocardial injury, and that non-ischaemic causes of myocardial injury( eg, takotsubo syndrome or myocarditis) have been excluded. 144
MINOCA accounts for about 6 % of MIs, and is more common in women, with studies reporting more than 50 %
145, 146 of those affected are women. While those with MINOCA have a more favourable prognosis than MI with obstructive CAD, the mortality from MINOCA is about 1 % in hospital, 2-5 % at one year, and about 11 % at five years 147, 148 MACE occurs in almost 25 % of those with MINOCA at four years. 149 The pathogenesis of MINOCA is heterogenous and includes atherosclerotic plaque rupture, plaque erosion, coronary spasm, coronary thromboembolism and, rarely, coronary dissection. 150 Box 6 lists the three-step diagnostic strategy for MINOCA. 151
The preferred treatment of MINOCA is medical; there is no established role for coronary stents in non-obstructive coronary plaque disruption. The impact of medical therapy for secondary prevention in MINOCA is unknown as clinical practice guidelines are largely based on patients with obstructive CAD. As MINOCA is a heterogenous condition, the best treatment varies according to the underlying cause but is yet to be proven. In addition, secondary prevention medications for MI are less often administered after a diagnosis of MINOCA. 152 Aspirin is recommended for secondary prevention in MINOCA, and dual antiplatelet therapy has not shown to be of benefit. 151, 153 Statins and ACE-I / ARB are associated with lower mortality and rates of MACE, and beta blockers with a trend towards benefit. 153-56 CCBs are reasonable in patients with coronary spasm as the mechanism of MI but have not been shown to reduce the long-term risk
153, 157 of MACE. Many patients have ongoing angina after an episode of MINOCA, so symptomatic antianginal treatment with beta blockers, CCBs or long-acting nitrates is often needed. CCBs are the most effective symptomatic therapy for VSA, followed by nitrates.
In patients with MINOCA and underlying heart failure with reduced ejection fraction( HFrEF), initiate treatments for heart failure. Recommend cardiac rehabilitation, which has been shown to reduce all-cause mortality and MACE in patients with MINOCA. 158
Adapted from Kunadian V et al 2020 24, Reynolds HR 2022 et al 90 Adapted from Reynolds HR et al 2022 90
Lifestyle factors and avoid precipitants
Nutrition, exercise, weight management, smoking cessation, stress management, cardiac rehabilitation
Consider statins and ACE-I
Continue to monitor status – symptoms or MACE.
ASCVD
Non-ischaemic causes of myocardial injury
Takotsubo
Myocarditis
Other cardiomyopathies
SPONTANEOUS CORONARY ARTERY DISSECTION
SCAD is an acute coronary event where the spontaneous development of an intramural haematoma, with or without an intimal tear, compresses the true vessel lumen leading to ischaemia and AMI. 159 Dissection can occur between any of the three layers of the arterial wall— intima, media or adventitia. It is a non-atherosclerotic problem that may cause narrowing and may be mistaken for MI from atherosclerosis and thrombosis. 160
Most patients with SCAD are women( 87-95 %), with an average age 44-53. 161, 162 They have lower rates of traditional risk factors than
Risk factor management Hypertension, dyslipidaemia, diabetes
Obstructive CAD
Antianginal therapy according to endotype
Microvascular angina 1. Beta blocker 2. Calcium channel blocker 3. Nicorandil 4. Ranolazine
Acute myocardial infarction( MI)
SCAD
* can also be non-obstructive
atherosclerotic patients with AMI; however, hypertension and hyperlipidaemia prevalence is similar to agesex matched populations. 163, 164 The prevalence of SCAD is estimated at 4 % of patients with an ACS but may account for 35 % of MIs in women 50
159, 165, 166 and younger.
Conditions associated with SCAD include those making coronary wall structures more prone to dissection, or stressors. 167 Peripartum is a predisposing condition, with SCAD the main cause of MI during pregnancy and postpartum. 168, 169 Fibromuscular dysplasia( FMD) is frequently associated with SCAD, so it is important to screen for this. There are associations with collagen vascular disorders( eg, Marfan and Ehlers-Danlos syndromes), chronic inflammatory
Vasospastic angina
1. Calcium channel blocker( 1st line, and cardioprotective)
2. Long-acting nitrate 3. Nicorandil 4. Ranolazine 5. Ivabradine
Figure 8. Management of INOCA.
Non-obstructive CAD MINOCA
Plaque rupture Plaque erosion
Microvascular dysfunction
Vasospasm Thrombosis Calcific nodule SCAD
Type 2 MI( supply demand mismatch)
Figure 9. Causes of acute myocardial infarction.
diseases( SLE, inflammatory bowel disease, sarcoidosis), susceptibility genes and migraine. 170-75 Apart from pregnancy, up to two-thirds of SCAD have precipitating triggers, most commonly extreme emotional or physical stress, recreational drugs or exogenous hormones. 159, 161, 176 Emotional stressors are more common precipitants in women, with physical
167, 177 stressors more common in men.
The presentation is similar to atherosclerotic AMI, with chest pain, elevated troponin and ECG changes( STEMI / NSTEMI), but in a different patient phenotype. Presenting features also include ventricular arrythmias, cardiogenic shock or sudden cardiac arrest. 178
Diagnosis requires careful attention to the coronary angiogram
Box 5. The management of suspected IHD
• Step 1:— Patient evaluation by GP: ischaemic symptoms, history including risk factors( traditional and non-traditional), physical examination, ECG.
• Lifestyle interventions and optimisation of CV risk factor control: nutrition, exercise, weight management, obesity, smoking cessation, stress management.
• Pharmacologic secondary prevention with GDMT to achieve and maintain CV treatment targets for BP, lipids and blood glucose.
• Hypertension: strict BP control prevents microvascular changes and reduces the frequency and intensity of anginal symptoms.
• Combination BP therapy depends on the mechanism with ACE-I improving CFR; ACE-I / ARB can be combined with beta blockers / CCBs.
• Dyslipidaemia: statins are beneficial in both obstructive and non-obstructive CAD and their anti-inflammatory properties may be effective in those with reduced CFR and vascular spasm.
• Start therapy for angina / angina equivalent.
• Consider cardiology referral.
• Step 2:— Non-invasive evaluation with functional or anatomic imaging to identify high risk subsets of stable CAD patients for whom revascularisation is more appropriate than medical therapy alone.
• Functional imaging: exercise stress test, stress echo, MIBI to look for ischaemia, PET / cardiac MRI to assess myocardial blood flow can help assess for CMD. Or
• CT coronary angiogram( CTCA).
• Step 3:— If functional imaging or CTCA confirms CAD:
• Optimise GDMT for CV event reduction.
• If very low angina threshold and / or left main disease suspected / large area of ischaemic myocardium, consider invasive coronary angiogram with or without functional assessment to identify left main, high grade / multivessel CAD.
• In all other chronic stable patients, an initial trial of empiric antianginal therapy is an important initial step and increasing doses and / or adding agents for symptom control( two antianginal drugs adjusted over 3-6 months), see table 2.
• Step 4:— Invasive coronary angiography and / or functional assessment:
• If ongoing symptoms, refer for coronary angiogram to identify flow-limiting stenoses that may benefit from revascularisation.
• In patients with ongoing symptoms and without obstructive CAD on coronary angiogram, consider functional assessment including FFR, CFR, IMR and acetylcholine testing for spasm, to guide further pharmacological management( see table 2).
Adapted from Boden WE et al 2023 18, Kunadian V et al 2020 24