Coronary Flow Effects of Arterial Spasm or Microembolization

Etiology

Coronary artery flow depends on the autonomic nervous system. The sympathetic nervous system activation will increase the effects of catecholamines, which will induce vasoconstriction and further decrease the blood flow. It is thought that coronary artery spasm can develop if there is unopposed alpha constriction.[4] The parasympathetic nervous system will not have a direct effect on spasm, but its reduced activity will promote more unopposed adrenergic activity, which can induce spasm.[5] Smoking, endothelial dysfunction, physical stress, and drugs like cocaine can also contribute to the development of spasm. Younger patients are more likely to develop spasm as compared to older patients. Genetic factors also contribute to the development of spasm.

Microembolization typically has associations with coronary artery disease with emboli originating from coronary plaques and obstructing the small vessels and distal circulation.[6]

Epidemiology

Coronary artery spasm is more common in the Japanese than in U.S. populations.[7] It is more common in women and the elderly than it is in men and the young. Its prevalence is higher in patients with an underlying coronary lesion. Some studies suggest that the decreased production of endothelial nitric oxide and autonomic dysfunction is more common in the Japanese population than in western countries and is responsible for the racial difference in coronary vasomotor activity. 

Pathophysiology

Rich innervation and muscularity of coronary vessels predisposed them to vasoactive effects of catecholamines as well as neuro-humoral system activation. As a result, inducement of coronary vasospasm can occur whenever there is a surge in circulatory catecholamines or when there is activation of the neurohumoral system.

Microembolization leads to increased resistance to flow across the coronary bed, which raises intracoronary pressures by vasoconstriction and impairs nutrient exchange as well as causing endothelial dysfunction, which results in ischemia.[3]

History and Physical

The patients usually present with sudden onset, pressure like radiating chest pain, which generally lasts for 5-20 minutes. The symptoms are recurrent and present in a similar way during each episode. If the symptoms do not respond to initial medical treatment, the patient can develop myocardial infarction or even sudden death. The classic presentation mimics typical angina pectoris, however resting pain with no pain between the episodes can be used to differentiate from classic angina pectoris.[8]

Physical examination should be performed to get baseline cardiovascular status to compare during the episodes. The patient can develop tachycardia, hypotension, or third heart sound during the episode, and return to baseline after the episode. If the right coronary artery is involved, the patient can develop bradycardia and hypotension because of the involvement of the nodal system and disruption of the blood supply to the right ventricle.

Evaluation

The best initial investigation is an electrocardiogram, which should be done in all patients presenting with chest pain. The findings vary from normal EKG to ST-segment changes, which will resolve either spontaneously or with treatment. Serial cardiac troponin testing is also indicated to rule out myocardial infarction. In a case where there are no EKG changes and patients have recurrent symptoms, ambulatory EKG can also be done to detect episodes of ST-segment elevation or depression with or without angina. Exercise has been shown to trigger spasms, so exercise testing can also be done to induce spasms once ECG and cardiac troponins have ruled out acute coronary syndrome (ACS). Stress tests combined with imaging will often yield perfusion defects/ ischemia in the territory of coronary artery suffering from spasmodic episodes. Invasive coronary angiography (ICA) will usually reveal non-obstructive coronaries, in which cases coronary functional testing via checking coronary flow reserve and coronary microvascular resistance is the next step, typically done by methods such as fractional flow reserve (FFR), coronary flow reserve (CFR), instantaneous wave-free ratio (iFR), and index of microcirculatory resistance (IMR). Provocative testing can be undertaken to look for coronary vasospasm. See Image. Coronary Flow Effects of Arterial Spasm or Microembolization. Invasive coronary angiography with provocative testing is the gold standard for the diagnosis.

Treatment / Management

Non-pharmacological treatment includes smoking cessation to prevent recurrent symptoms.

Pharmacological management depends on the presentation and the EKG changes. Nitrates will help in reducing symptoms, but coronary angiography should be done to rule out active coronary lesions. If coronaries are normal, long-acting nitrate with or without calcium channel blocker will improve the symptoms. In acute attacks, sublingual nitrates can also be used to get an immediate effect. Calcium channel blockers have vasodilating properties and can be used to prevent recurrent attacks. The dose should be gradually increased to reach the maximal tolerable dose. Beta-blockers should be avoided as it increases the risk of spasm, but if the patient has left ventricular (LV) dysfunction, then beta-blocker will need to be instituted considering the associated mortality benefit. ICD should also be a consideration in patients for secondary prevention.[9]

Differential Diagnosis

• Unstable angina
• Myocardial infarction
• Coronary artery anomalous origin
• Pulmonary embolism
• Aortic dissection
• Esophageal spasm

Prognosis

The prognosis of coronary spasm is good if promptly recognized, and patients usually respond well to medical management.

Microembolization on the other end doesn't respond very well to treatment especially in the setting of ACS or coronary intervention. It usually leads to microvascular dysfunction.

Complications

1. Myocardial infarction

2. Myocardial dysfunction

3. Arrhythmias (ventricular tachycardia or fibrillation)

4. Sudden cardiac death

5. Acute pulmonary edema

6. Heart failure