Coronary Slow Flow and Acute Coronary Syndrome in a Patient with Spinal Cord Injury

Abstract

We report the case of a 55-year-old man who presented with acute coronary syndrome due to coronary slow flow after spinal cord injury. Data regarding the causes and clinical manifestations of coronary slow flow are inconclusive, but the autonomic nervous system is believed to be at least a contributing factor. The predominant vagal activity causes vasodilation and hemostasis, which can lead to acute coronary syndrome. We hereby call attention to hyperactive parasympathetic tonicity, which can lead to coronary slow flow and acute coronary syndrome in acute spinal cord injury patients.

WEB SITE FEATURE

The phenomenon of coronary slow flow as observed during coronary angiography is characterized by delayed opacification of the distal coronary segments in the absence of epicardial coronary disease. This “spontaneous” coronary slow flow is thought to be caused by endothelial dysfunction that upsets the balance between coronary vasodilation and vasoconstriction.¹ Among the important determinants of coronary blood flow are endothelium-derived vasoactive factors, the autonomic nervous system, angiotensin II, autocoids (histamine and bradykinin), metabolic messengers (carbon monoxide and pH, adenosine, and adenosine triphosphate), and potassium channels.² Information about the cause and clinical manifestations of coronary slow flow is inadequate, but the autonomic nervous system is thought to contribute.²

The acute phase of spinal cord injury (SCI) can cause certain cardiovascular sequelae. For example, the anatomic or physiologic disruption of supraganglionic intraspinal sympathetic fibers can reduce vascular tonicity and stimulate vagal hyperactivity. The components of predominant vagal activity include vasodilation and hemostasis,³ which can lead to acute coronary syndrome (ACS). To our knowledge, our case is the first in the medical literature that shows ACS with coronary slow flow in a patient with SCI.

Case Report

In December 2009, a 55-year-old man with paraplegia presented with acute crushing pain and a sensation of weight on his chest, experienced at rest. He had only recently been discharged from the neurology department of a state hospital, where he had been treated for a traumatic spinal cord injury sustained 9 days earlier. He had no chronic disease, such as hypertension or diabetes mellitus, and he maintained that he had been perfectly healthy before the accident.

On admission, the patient exhibited passive posture due to his paraplegia; he appeared to be anxious but said that his pain had eased. His blood pressure was 105/80 mmHg, his heart rate was 72 beats/min, and his cardiac and pulmonary auscultatory results were normal. His initial 12-lead electrocardiogram (ECG) seemed normal, but his serum troponin I level was 0.1 ng/mL (normal range, 0–0.06 ng/mL). He was hospitalized in order to monitor possible alterations in the cardiac marker or the ECG. There was also a consultation with neurology, and magnetic resonance imaging of the patient's spine revealed high signal intensity from C3 through C6 (Fig. 1).

Fig. 1 Magnetic resonance imaging reveals a high-signal area (large arrow) indicative of spinal cord injury at the C3 through C6 levels.

During the hospital stay, the patient again experienced crushing chest pain and was re-evaluated. His physical examination was normal, but 12-lead ECG revealed ST-segment alterations in leads V₁ through V₄ in the absence and presence of chest pain (Figs. 2A and 2B, respectively). The serum troponin I level remained at 0.1 ng/mL, and the myocardial band fraction of creatine kinase was 2.6 U/L (normal range, 2–14 U/L). Septal and anterior hypokinesia without apical ballooning was observed upon echocardiography. The patient's chest pain and dynamic ECG alterations were regarded as unstable angina pectoris, for which we performed emergency coronary angiography. Coronary flow velocity was observed to be decelerated in the absence of significant stenosis (Fig. 3A). The Thrombolysis in Myocardial Infarction (TIMI) frame-count method was used to evaluate the degree of the slow antegrade filling. The corrected TIMI frame counts were observed to be 41 frames for the left anterior descending coronary artery (LAD). Coronary angiography revealed no significant stenosis in the right coronary artery (RCA) (Fig. 3B). Observed TIMI frame counts were 26 for the RCA and 36 for the left circumflex coronary artery (LCx) (Fig. 3C).

Fig. 2 A) Electrocardiogram shows ST-segment alteration in leads V₁ through V₄ during absence of chest pain. B) Electrocardiogram shows ST-segment elevation in leads V₁ through V₄ during presence of chest pain.

Fig. 3 A) Coronary angiogram (right anterior oblique projection) reveals no significant stenosis, together with coronary slow flow in the left anterior descending coronary artery. B) Coronary angiogram reveals no significant stenosis in the right coronary artery. C) Coronary angiogram (right anterior oblique cranial projection) reveals no significant stenosis, together with coronary slow flow in the left anterior descending coronary artery.

Real-time motion images are available at www.texasheart.org/journal.

A calcium-channel blocker and warfarin were administered, together with routine anti-ischemic agents. After the onset of treatment, the patient did not experience a 3rd episode of angina, and his ST-segment alterations returned to normal. The patient was transferred to the state hospital's rehabilitation unit for his spinal cord injury. After physical therapy, he was ambulatory and did not experience angina.

Discussion

The coronary resistance vessels are richly innervated by the parasympathetic division of the autonomic nervous system,⁴ and that system modulates coronary blood flow.²

Cardiovascular diseases in patients with SCI occur most often in the acute stage of the initial injury.^5–7 Disruption of the supraganglionic intraspinal sympathetic fibers can reduce vascular tonicity and stimulate vagal activity. Such vagal system activity causes vasodilation and hemostasis, as well as bradycardia and hypotension.³ Low resting blood pressure and orthostatic hypotension more often occur in patients who have severe SCI at the cervical or high-thoracic (T6 or above) level.^8,9 These patients also can experience sudden episodes of extremely elevated blood pressure, accompanied by other signs or symptoms of autonomic overactivity in response to stimuli below the level of injury (so-called “autonomic dysreflexia”).¹⁰ In addition, acute SCI can provoke thromboembolic events and increase susceptibility to cardiac arrhythmias. Excessive parasympathetic activity might be related to coronary slow flow and ACS in patients with SCI.

Cardiac adrenergic signals are observed to contribute to the regulation of myocardial blood flow. According to Di Carli and colleagues,¹¹ hydroxyephedrine (an analogue of norepinephrine) showed greater uptake in the LAD territory than in the territories of the RCA and the LCx; and the increase in blood flow in response to cold pressor testing was also higher in the territory of the LAD (46% ± 10%) than in that of the RCA (16% ± 5%; P = 0.01) or the LCx (23% ± 16%; P = 0.06). Further, Di Carli's group suggested that increases in coronary blood flow in response to sympathetic stimulation correlate with the regional norepinephrine content in the cardiac sympathetic-nerve terminal, and that cardiac adrenergic signals play an important role in the regulation of myocardial blood flow.¹¹ This mechanism might contribute to the slow-flow phenomenon as monitored in the LAD territory only.

It has been reported that coronary slow flow can lead to ischemia and angina pectoris, but slow flow is not an incidental angiographic finding.^12–15 Beltrame and colleagues¹⁶ have reported that mibefradil (a calcium T-channel blocker) improves the velocity of coronary blood flow. Increased vagal tonicity might be the main cause of velocity deceleration and hemostasis. It is recommended that anticoagulants be continued until hospital discharge in patients with incomplete SCI, and for 2 months in patients with uncomplicated, complete SCI.

Abnormal ECG findings, especially ST elevation, are frequently observed in the acute stage of SCI.^17,18 High vagal tonicity is currently considered the major contributing factor.¹⁹ Recognition of this early repolarization pattern is important in the differential diagnosis of myocardial infarction or pericarditis.³ The duration of the sympathetic imbalance in the acute phase is usually 2 to 3 weeks. During the period of excessive vagal tonicity, it is crucial to avoid any provocation that may lead to further vagal activation or enhancement of vasovagal reflexes. Atropine should be kept handy, even at the patient's bedside. Parasympatholytic agents might be beneficial in the treatment of coronary slow flow and ACS in patients with SCI. Conversely, angiotensin-converting enzyme inhibitors should be avoided in such patients, because of the prolonged activation of the renin, angiotensin, and aldosterone system.

In summary, patients with acute-stage SCI can experience coronary slow flow (and consequent ACS) due to increased parasympathetic activity. Awareness of this phenomenon is important in the differential diagnosis of chest pain, and during early treatment and follow-up of ACS.