Classically, chronic intestinal angina is caused by a reduction in mesenteric blood flow [
1], and the pathophysiology of most cases is atherosclerotic stenosis of the celiac and mesenteric arteries. Arterial dissection, fibromuscular dysplasia, and vasculitis are included as rare etiologies of arterial narrowing, and the median arcuate ligament of the diaphragm can compress the celiac artery and disturb blood flow (median arcuate ligament syndrome) [
5,
6]. Intestinal circulation consists of an abundant collateral blood supply, and chronic intestinal ischemia is associated with high-grade stenosis or occlusion of two or more of the three major vessels: the celiac artery, the superior and inferior mesenteric arteries [
7,
8]. In our case, the arterial lesions were relatively mild compared with previous reports [
9,
10]; thus, we hypothesized that our patient’s major symptoms were not due to his arterial lesions alone.
Specifically, our patient’s symptoms depended greatly on his hemodynamic condition, which caused a flow discrepancy between demand and supply [
1]. Once an abdominal attack occurred, our patient’s blunted oral intake exacerbated repetitive postprandial attacks; only fluid replacement led to remission. Furthermore, advanced AV block abruptly worsened his condition and pacemaker implantation with right ventricular apical pacing resulted in complete remission of his symptoms. In patients with HOCM, dehydration augments LVOT obstruction and mitral regurgitation, leading to reduced cardiac output [
2]. Pacemaker implantation with right ventricular apical pacing increases cardiac output by optimizing chronotropic action as well as by lowering the LVOT gradient in HOCM patients [
11,
12]. Nonocclusive mesenteric ischemia is a type of intestinal ischemia attributed to hemodynamic failure, sometimes without arterial stenosis or occlusion. Vasospasm of mesenteric vessels is assumed to be a major pathophysiological and acute homeostatic response used to maintain systemic circulation at the expense of the splanchnic blood supply in critically ill conditions, such as cardiogenic shock [
13]. In our case, the patient complained mainly of long-standing postprandial abdominal pain without any signs of severe circulatory failure in other organs. He was later diagnosed with uncontrolled HOCM complicated with stenosis of the celiac and mesenteric arteries, and his symptoms reflected excessive hemodynamic fluctuation specific to HOCM. Generally, easily digestible meals or vasodilators are used as supportive therapy, while the definitive treatment for intestinal angina is revascularization by surgery or catheterization [
13]. However, our patient was too old and emaciated to undergo these invasive treatments. Although he underwent pacemaker implantation, it was less invasive than was revascularization therapy. HOCM is commonly treated with oral medications, such as calcium channel blockers, β-adrenoreceptor blockers, and antiarrhythmic agents included in group Ia of the Vaughan-Williams criteria, to reduce myocardial oxygen consumption and inhibit left ventricular hypercontraction. Percutaneous transluminal septal myocardial ablation, septal myectomy, and pacemaker implantation are other potential treatments if oral therapy is not successful. Although the efficacy of septal myectomy in improving the long-term prognosis of HOCM patients was reported previously [
14], this treatment is well known for its high mortality rate, with older age being a risk factor [
15]. In this case, pacemaker implantation was selected as the treatment, because our patient’s systemic circulation and abdominal symptoms were clearly exacerbated by bradycardia from AV block.
Some limitations were observed in this case report. No intestinal hemodynamic parameters were evaluated, because abdominal ultrasound was unable to detect the celiac and mesenteric arterial flows. Furthermore, our patient was very emaciated and unable to undergo catheter examination. However, after pacemaker implantation, his symptoms, intestinal dilatation, and renal function improved without fluid replacement or additional medications, which reflected improvement of his systemic circulation.