Hypovolemia-induced severe coronary spasm leading to acute myocardial infarction

Abstract

Acute ST-elevation myocardial infarction (STEMI) is a well recognized manifestation of severe coronary artery spasm. Although there are many recognized triggers, hypovolemia has not been previously described. The present report describes a case of acute STEMI that occurred four days following major colonic surgery in a severely dehydrated patient. Coronary angiography revealed underfilled coronary arteries with severe multifocal spasm, which largely resolved with aggressive fluid repletion and intracoronary nitrate.

Acute ST-elevation myocardial infarction (STEMI) is a well recognized manifestation of severe coronary artery spasm. Although there are many recognized triggers of STEMI, hypovolemia has not been previously described. We describe a case of acute STEMI that occurred four days after major colonic surgery in a severely dehydrated patient. Coronary angiography revealed underfilled coronary arteries with severe multifocal spasm, which largely resolved with aggressive fluid repletion and intracoronary nitrate.

CASE PRESENTATION

A 78-year-old male smoker with a medical history of hypertension presented with nausea, dyspnea and diaphoresis four days after an anterior resection operation for a colonic adenocarcinoma. The patient’s cancer had been diagnosed two months earlier and he was treated with a course of radiotherapy followed by the aforementioned surgical procedure, which included a defunctioning colostomy. He had lost a substantial amount of blood intraoperatively. On examination, he appeared pale, clammy and peripherally shut down. He was tachycardic, with a heart rate of 112 beats/min and a blood pressure of 99/60 mmHg. His respiratory rate was 33 breaths/min and his oxygen saturation was 92% on 4 L oxygen. Cardiopulmonary examination revealed normal heart sounds, no murmurs and clear lung fields. Abdominal examination revealed a healthy midline scar with no evidence of bleeding or infection. There was some generalized abdominal tenderness with absent bowel sounds but no guarding. There was minimal drainage through the intra-abdominal drain and the stoma bag was empty. A small amount of dark, concentrated urine was present in his urinary bag. Inspection of the fluid chart revealed him to be in a net negative balance of at least 5 L over the preceding four days. An electrocardiogram (ECG) revealed sinus tachycardia with mild ST segment elevation in the inferolateral leads, which was not present on his preoperative ECG (Figure 1). Transthoracic echocardiography revealed good left ventricular systolic function with no obvious wall motion abnormalities. Blood tests revealed a hemoglobin level of 96 g/L, a white blood cell count of 11.7×10⁹/L, a platelet count of 298×10⁹/L, and urea, creatinine and C-reactive protein levels of 13.5 mmol/L, 141 μmol/L and 140 mg/L, respectively.

Figure 1).

Baseline electrocardiogram (ECG) (left panel) compared with electrocardiogram at time of index event demonstrating ST segment elevation in the inferolateral leads (right panel)

An acute inferolateral STEMI was diagnosed, and the patient was preloaded with acetylsalcylic acid 300 mg and clopidogrel 600 mg and transferred to the cardiac catheterization laboratory for emergent coronary angiography. The procedure was performed via a right femoral artery approach using standard equipment. The initial intra-arterial pressure was 90/60 mmHg. Left ventricular (LV) angiography revealed a small, underfilled left ventrical (Figure 2) with vigorous contraction and no obvious wall motion abnormalities. Selective coronary angiography (Figures 3 and 4) revealed generally low calibre, atretic vessels, with multiple stenoses in all major epicardial vessels. The most severe of these apparent lesions were in the proximal and distal one-third of the right coronary artery, which explained the ECG findings. Because of the multifocal nature of the lesions, the generally underfilled appearance of the coronary arteries and the small, vigorously contracting left ventricle, hypovolemia-induced coronary spasm was postulated as an underlying mechanism for the coronary angiographic appearance. The patient was rehydrated aggressively with intravenous gelofusine (B Braun, Germany) and he received multiple 200 μg boluses of glyceryl nitrate into each coronary system. Repeat coronary angiography revealed a significant increase in coronary artery calibre with almost complete resolution of all coronary stenoses, apart from mild residual plaque disease in the distal right coronary artery (Figure 5) and distal left anterior descending artery (Figure 6). Concurrent with the above was complete resolution of the ST segment elevation in the inferolateral leads. No coronary intervention was deemed necessary and the patient was managed conservatively on the coronary care unit where his condition remained stable over the following 48 h. A 12 h troponin T level was elevated at 1.33 ng/mL. He continued to make good progress under the care of the surgical team.

Figure 2).

Small, vigorously contracting left ventricle

Figure 3).

Severe multiple stenoses in underfilled right coronary artery

Figure 4).

Severe multiple stenoses in underfilled left coronary artery

Figure 5).

Right coronary artery following fluid repletion and intracoronary nitrate showing an increase in vessel calibre and resolution of coronary spasm

Figure 6).

Left coronary artery following fluid repletion and intracoronary nitrate showing an increase in vessel calibre and resolution of coronary spasm

DISCUSSION

Coronary spasm is a well recognized cause of angina, a syndrome also known as prinzmetal, vasospastic or variant angina (1,2). This syndrome may be associated with ST segment elevation and, when the spasm is severe or prolonged, myonecrosis. The pathophysiology of this syndrome is most likely related to an abnormality of normal vasodilator function within the coronary arteries and/or hypersensitivity of the coronary arteries to normal mediators of vasoconstriction. Known triggers of prinzmetal angina include smoking, thyroid dysfunction, collagen disorders and recreational drug use such as cocaine, amphetamines and ethanol.

In the present case, we describe another potential trigger of coronary artery spasm, namely hypovolemia. There was clear evidence of a mismatch between fluid input and output in the present case, leading to a state of dehydration in the early postoperative period. This manifested as hypotension, a rise in serum urea and creatinine levels, and poor urine output. We believe that this state of dehydration led to coronary underfilling, which precipitated severe coronary spasm. Supporting this were multiple lesions in both coronary systems, which largely resolved with fluid repletion and intracoronary nitrate. Although the coronary spasm was sufficiently severe to cause myonecrosis, it was presumably not prolonged enough to result in any discernible reduction in LV systolic function due to the dynamic nature of coronary spasm.

The prognosis of patients with myocardial infarction caused by prolonged coronary spasm in the absence of significant coronary artery disease is generally good (3,4). Coronary vasospasm generally responds to calcium channel blockers and nitrates; however, prolonged spasm can cause life-threatening arrhythmias that can be fatal (5). In such cases, high doses of both calcium channel blockers and vasodilators, along with device support, may be indicated.

In summary, the present case documents hypovolemia as a potential cause of coronary artery spasm leading to STEMI. Clinicians should be vigilant to this possibility in all patients presenting with STEMI in the postoperative period when a state of severe dehydration is often present. Adequate rehydration and meticulous attention to fluid balance in the perioperative period are essential to prevent this complication.