Angina and Myocardial Infarction Without Significant Coronary Stenosis

• Myocardial Infarction and Unstable Angina with Absence of Significant Angiographic Stenosis
• Overview
• Severe Reversible Acute Cardiomyopathy Secondary to Severe Stress
• Coronary Spasm and Myocardial Infarction or Unstable Angina

Chest pain in the absence of significant coronary disease

It is not uncommon to see patients with chest pain who subsequently are found to have no significant disease at coronary angiography. Clinical studies have shown that, as a group, these patients to have a good prognosis.

• Single episode of severe and prolonged angina like discomfort with elevation of cardiac troponins.
• Angina like chest pain predominantly occuring with exercise and relieved by rest, but sometimes also occuring at rest, and usually responsive to nitrolingual spray.
• Chest discomfort that is persistent, and fluctuates in intensity during the day and also from week to week.
• Clearly atypical chest pain for angina and suggestive of musculoskeletal discomfort.

Most would agree that some of these patients clearly have cardiac ischaemia as the cause of their chest pain, but possibly the majority of patients have non-ischaemic chest pain. Altered pain threshold levels may also be a factor in some patients.

Chest pain with elevated troponin levels but without significant coronary disease

It is not uncommon to see patients who present to hospital after having had their first episode of prolonged angina like chest pain, with elevation of cardiac troponins and in the absence of any confounding factors such as surpraventricular tachycardias.

Many of these patients also develop T waves changes, such as biphasic T wave abnormalities that then progress to symmetrical T inversion consistent with chest pain being secondary to cardiac ischaemia.

The chest pain many occur in the setting of chronic stress or even in the setting of sudden severe emotional stress. We have now seen numerous instances of chest pain occuring in relation to severe emotional stress with associated troponin elevation and with either angiographically normal coronary arteries or with minor disease only.

The routine use of troponin testing and increased use of coronary angiography has undoubtedly improved our recognition of this condition.

In my experience, most of these patients do not go onto have recurrent problems with chest pain or recurrent admissions to hospital with prolonged chest pain.

In the early experience of troponin testing, it was not uncommon for the "positive" troponin results to be dismissed as being false or to blame the particular troponin assay being used as being inaccurate- yet many of these troponin elevations had the typical rise and fall seen in acute coronary syndromes.

One wonders if some of these patients might have had an isolated episode of coronary artery spasm. In other patients, especially those with some mildly stenotic lesions present, the episode may be due to embolisation from these mild lesions of small thrombi.

Exertional angina but with no significant obstructive coronary artery disease

Such patients almost always respond to use of sublingual nitrates. This tends to indicate a high chance of response to high dose oral nitrates and oral calcium channel blockers.

It is not uncommon to see this group of patients. Some have impressively positive treadmill stress tests for symptoms and ECG changes, others only develop chest pain and not ECG changes.

One wonders if these patients have an abnormal coronary vasomotor response that is responsive to nitrates and calcium channel blockers. One tends to assume there is endothelial dysfunction that will improve with use of statin therapy. It is possible that amongst this group will be some with obvious musculoskeletal causes of chest pain.

Persistent mild chest discomfort that bears little relationship to activity

If these patients find sublingual glyceryl trinitrate to be helpful then a trial of therapy with oral nitrates and calcium channel blockers should be considered. Generally, however, this treatment does not seem to work.

Some of these patients may be admitted to hospital repeatedly, but cardiac troponin levels do not increase. Repeated hospital admissions with severe and prolonged chest pain, but with failure of troponin elevation to occur, should strongly suggest the non-cardiac basis of the chest pain syndrome. The complicating factor is that some of these patients also have coronary artery disease and can end up having percutaneous intervention or coronary bypass surgery which do not provide any lasting relief from symptoms.

Often empiric therapy with acid suppressant medication such as omeprazole can be tried. I tend to do this first, rather than to refer for oesophageal manometry studies.

Not infrequently, these patients admit to having significant psychosocial stressors that might be the cause of chest pain.

Final Comments

Most would agree that some of these patients clearly have cardiac ischaemia as the cause of their chest pain, but possibly the majority of patients have non-ischaemic chest pain. Altered pain threshold levels may also be a factor in some patients. If there is no other non-cardiac cause of chest pain, the focus should be on control of cardiac symptoms and reassurance of the patient.