Though data on the incidence of thromboembolic specific AMI have generally been limited to individual case series, a Swedish population-based autopsy study by Acosta et al has shed considerable light on this area. In Malmo, Sweden, a community in which 87 % of deaths are investigated by autopsy, 213 cases of thromboembolic AMI were identified from over 30,000 autopsies performed from 1970 to 1982; these were then added to the number of operations performed for AMI at the lone Malmo regional hospital over a 3-year sample period to produce a thromboembolic AMI incidence of 8.6 cases per 100,000 person-years [22]. Median age of those who died from thromboembolic AMI was 81 years with two thirds of cases being female. Incidence of AMI nearly doubles with each 5-year interval above age 70 with an incidence of 25 cases per 100,000 person-years for ages 70–74 that then rises to an incidence of 217 cases per 100,000 person-years for patients greater than 85 years. Interestingly, adjustment for the greater longevity of females in this population showed that female gender was not, in fact, an independent risk factor for AMI in this cohort.

The epidemiology of thromboembolic AMI may be influenced by the prevalence of conditions that place patients at increased risk. The pathophysiology of thrombotic AMI suggests that conditions such as prior cerebrovascular accident, aortic wall thrombosis, disseminated cancer, and CMI may increase risk of thrombotic events [20]. Not surprisingly, case series on AMI have documented rates of preexisting CMI in 0–43 % of cases [20, 23–25]. Risk for embolic AMI is increased by comorbid conditions suggestive of prior embolic events such as cerebrovascular accident or predisposing to embolic events including atrial fibrillation, congestive heart failure, and recent myocardial infarction among others [26]. A report by Batellier and colleagues on 82 consecutive patients treated for SMA embolism over a 22-year period (1966–1988) demonstrated a history of atrial fibrillation in 79 % (N = 65/82) of cases and a history of prior embolic event in 35 % (N = 29/82) [25]. Accordingly, autopsy study of 122 patients with AMI attributable death showed a cardiac source of thrombus in approximately half of cases (N = 58/122) [27]. As the management of atrial fibrillation improves with better adherence to anticoagulation guidelines, it is hypothesized that the incidence of embolic AMI may also decrease though population level in this regard is lacking [26, 28]. Data from the National Health and Nutrition Examination Survey (NHANES) database supports this possibility as it demonstrates a sharp increase in the use of aspirin, clopidogrel, warfarin, and statin drugs over the period from 1999 to 2010 [8].

Mesenteric Venous Thrombosis – MVT is encountered in the acute form, which commonly presents as bowel infarction, or the chronic form, which may present more insidiously with nonspecific symptoms or esophageal varices in cases with portal vein involvement. Here we will focus on acute MVT. Again looking toward clinical and autopsy data from Malmo, Sweden, study periods from 1970 to 1982 and 2000 to 2006 showed a rising incidence of mesenteric venous thrombosis (MVT) with 2.0 cases per 100,000 person-years in the earlier period as compared to 2.7 cases per 100,000 person-years seen in the latter, this on the basis of 63 (56 % autopsy) and 51 (12 % autopsy) identified MVT cases, respectively [29, 30]. A rise in the use of abdominal imaging has certainly contributed to increased MVT detection as 69 % of patients in the period 2000–2006 were diagnosed with CT scan as compared to 0 % in the earlier period. Even within the period 2000 to 2006, a greater proportion of cases were diagnosed by CT scan in the latter half (2004–2006: N = 10/21) than in the former (2000–2003: N = 25/30); p = 0.026. With an increasing proportion of cases diagnosed by cross-sectional imaging, it is likely that these data represent an increase in detection rather than an increase in true incidence. MVT involved secondary thrombus, or those cases in which an etiologic factor has been identified, in a majority of cases (80 %). As our understanding of congenital and acquired thrombotic states improves, the number of MVT cases attributed to primary thrombus, or those of unidentified etiology, has decreased [31]. Though men and women were equally likely to develop MVT, advancing age was correlated with increased incidence of MVT with septuagenarians having over twice the risk of those aged 60–69 years, 11.3 vs. 4.8 cases per 100,000 person-years, respectively. Approximately two thirds of these patients (N = 34/51) were noted to have either a congenital or acquired thrombophilia with the remainder having either intra-abdominal infection or other pro-thrombotic conditions such as pancreatitis (18 %), post-surgical trauma (8 %), or inflammatory bowel disease (2 %). Rhee et al from the Mayo Clinic published on 72 cases of MVT (57 acute) from 1972 to 1993 with findings largely in agreement with the Swedish data [32]. Similar rates of secondary thrombus (75 %) were seen, and again thrombophilia or prior surgery were among the leading causes of MVT. CT scan was abnormal in all patients with acute MVT who were studied. Though rare, acute MVT diagnosis has increased over time owing to the improved quality and increased use of intra-abdominal vascular imaging.

As the name would imply, NOMI refers to intestinal gangrene in the setting of patent mesenteric vessels [33]. First described in a 1949 case report from the Massachusetts General Hospital [34], NOMI describes a clinical syndrome comprising a number of entities which share the common pathophysiologic elements of mesenteric vasoconstriction, intestinal hypoxemia, ischemia–reperfusion injury, increased intestinal metabolic demand, and infection [35]. One in 5,000 hospital visits is attributed to NOMI [19] though given its nebulous description and frequent association with other pathologies, the true incidence may be difficult to define. Autopsy data from Sweden by Acosta and colleagues demonstrated an incidence of 2.0 cases per 100,000 person-years for fatal NOMI with incidence in octogenarians noted to increase to 40 cases per 100,000 person-years [36]. Nested case–control comparisons with non-NOMI autopsy patients identified fatal heart failure, history of atrial fibrillation, and recent surgery to be risk factors for fatal NOMI. Mesenteric stenosis also appears to have an association with NOMI as 25 of 62 patients in this series showed SMA stenosis at autopsy, with 14 of those also having celiac stenosis. Yet, importantly, the critical aspect in the development of NOMI is a low flow state, a state that may occur with or without concurrent mesenteric stenosis. Beyond these few epidemiologic studies, data on NOMI are primarily drawn from small case series and case reports relating it to varied conditions associated with either profound isolated vasoconstriction (e.g., cocaine use, digitalis toxicity) or low flow states with or without critical illness and vasopressor support [37–41].