Circadian Variation of Myocardial Ischemia in Patients with Stable Coronary Artery Disease

The circadian variation of myocardial ischemia detected during 24-h ambulatory electrocardiographic monitoring (AEM) was analyzed in 123 patients with stable angina pectoris, positive exercise test, and angiographically proven coronary artery disease. A total of 437 ischemic episodes (ST-segment depression ≥ 1 mm and duration ≥ 1 min) were observed; 333 (76%) episodes remained asymptomatic, and only 104 (24%) episodes were accompanied by anginal pain. Ischemic episodes predominantly occurred during the morning hours, between 6 a.m. and noon, and another smaller peak was observed in the afternoon, between 4 and 5 p.m.; this diurnal pattern was influenced neither by the extent of coronary artery disease nor the degree of left ventricular dysfunction. The circadian variation was restricted to the 345 (78%) ischemic episodes preceded by increases in heart rate; the 92 (22%) episodes without prior heart rate changes occurred randomly throughout the day. The morning peak in ischemic episodes was not associated with less myocardial oxygen supply; in contrast, heart rate profile showed parallel increases during the morning and afternoon hours, indicating elevated myocardial demand during these periods. Ischemia-related ventricular arrhythmias were concentrated during the morning hours, but their overall prevalence was low–28 (6%) of 437 ischemic episodes. These findings may provide further insight into the pathomechanisms of acute clinical events in patients with coronary artery disease, since the circadian variation of myocardial ischemia is very similar to that observed for the onset of myocardial infarction and sudden cardiac death.     

Circadian Variation of Myocardial Ischemia in Patients with Stable Coronary Artery Disease

The circadian variation of myocardial ischemia detected during 24-h ambulatory electrocardiographic monitoring (AEM) was analyzed in 123 patients with stable angina pectoris, positive exercise test, and angiographically proven coronary artery disease. A total of 437 ischemic episodes (ST-segment depression ≥ 1 mm and duration ≥ 1 min) were observed; 333 (76%) episodes remained asymptomatic, and only 104 (24%) episodes were accompanied by anginal pain. Ischemic episodes predominantly occurred during the morning hours, between 6 a.m. and noon, and another smaller peak was observed in the afternoon, between 4 and 5 p.m.; this diurnal pattern was influenced neither by the extent of coronary artery disease nor the degree of left ventricular dysfunction. The circadian variation was restricted to the 345 (78%) ischemic episodes preceded by increases in heart rate; the 92 (22%) episodes without prior heart rate changes occurred randomly throughout the day. The morning peak in ischemic episodes was not associated with less myocardial oxygen supply; in contrast, heart rate profile showed parallel increases during the morning and afternoon hours, indicating elevated myocardial demand during these periods. Ischemia-related ventricular arrhythmias were concentrated during the morning hours, but their overall prevalence was low-28 (6%) of 437 ischemic episodes. These findings may provide further insight into the pathomechanisms of acute clinical events in patients with coronary artery disease, since the circadian variation of myocardial ischemia is very similar to that observed for the onset of myocardial infarction and sudden cardiac death.     

Therapeutic potential of vitamin E against myocardial ischemic-reperfusion injury.

Myocardial ischemia is a disease process characterized by reduced coronary flow such that the supply of nutritive blood to heart muscle (myocardium) is insufficient for normal myocardial aerobic metabolism. Prompt reestablishment of coronary flow by invasive and noninvasive clinical procedures is the most direct and effective means of limiting myocardial damage in ischemic heart disease patients, although reperfusion carries with it an injury component which may reflect, at least to some degree, the toxic effects of partially reduced oxygen species and their participation in degenerative cellular processes such as membrane lipid peroxidation. Vitamin E, a lipophilic, chain-breaking antioxidant, is a prominent membrane constituent in heart muscle, where it modulates/regulates various aspects of heart muscle-cell metabolism and function. Vitamin E's beneficial effects against experimentally induced oxidative damage to the heart, along with inverse epidemiological correlations between plasma vitamin E level and either anginal pain or mortality due to ischemic heart disease, suggest that vitamin E might have protective and therapeutic roles against myocardial ischemic-reperfusion injury. Laboratory investigations aimed at addressing this possibility have demonstrated that vitamin E supplementation protects isolated hearts against ischemic-reperfusion injury, and relatively more inconsistent and limited data document cardioprotective effects of vitamin E in some animal models of myocardial ischemia-reperfusion, especially when administered prior to the ischemic period. Clinical attempts to establish whether vitamin E has therapeutic benefit in ischemic heart disease patients remain inconclusive, having relied upon a variety of nonuniformly controlled protocols and a single, rather subjective endpoint (anginal pain). Consequently, although laboratory data constitute a conceptual context for and indirect support of the idea that vitamin E could be a cardioprotectant against ischemic-reperfusion injury, compelling clinical evidence regarding vitamin E's therapeutic potential in the ischemic heart-disease patient is lacking. Elective coronary revascularization would appear to provide an attractive clinical setting for evaluating the therapeutic efficacy of vitamin E in the context of cardiac ischemia-reperfusion. Further biochemical work would still be required to define how vitamin E exerts any cardioprotective effect observed in these patients.     

Results of 14 Years' Experience in the Surgical Treatment of Human Coronary Artery Insufficiency

Atherosclerosis obstructs the main stems of coronary arteries, restricting the coronary artery inflow tract. Nature develops intramyocardial collaterals but fails to form extracoronary collateral channels. It is only through surgical measures that extracoronary collateral channels may be formed, for example, by internal mammary artery implantation and omental graft without pedicle operations. Preoperative assessment, with particular reference to anginal pain, disease activity, indications for and contra-indications to surgery, is outlined. The importance of cine coronary arteriography is stressed. The results of internal mammary artery implantation with or without omental graft in patients followed up for two to 14 years are presented. Operative mortality in 103 consecutive patients was 2.9%. There was marked improvement in over 70% of 115 patients reviewed. Post-operative examination of 29 implanted internal mammary arteries showed that 76% were open when examined up to 10 years postoperatively; many of these were studied by cineangiography.     

The appropriate use of carotid endarterectomy

FOR THE FIRST 30 YEARS AFTER CAROTID ENDARTERECTOMY WAS FIRST DEVELOPED, anecdotal evidence was used to identify patients with internal carotid artery disease for whom this procedure would be appropriate. More recently, the appropriateness of carotid endarterectomy for symptomatic patients and asymptomatic subjects has emerged from 7 randomized trials. Risk of stroke and benefit from the procedure are greatest for symptomatic patients with at least 70% stenosis of the internal carotid artery. Within this group, carotid endarterectomy is most beneficial for the following patients: otherwise healthy elderly patients, those with hemispheric transient ischemic attack, those with tandem extracranial and intracranial lesions and those without evidence of collateral vessels. Risk of perioperative stroke and death is higher in the following groups, although they still benefit: patients with widespread leukoaraiosis, those with occlusion of the contralateral internal carotid artery and those with intraluminal thrombus. Patients with 50% to 69% stenosis experience lesser benefit, and some other groups may even be harmed by carotid endarterectomy, including women and patients with transient monocular blindness only. The procedure is indicated for patients presenting with lacunar stroke and for those with a nearly occluded internal carotid artery, but the benefit is muted. Patients with less than 50% stenosis do not benefit. In the largest randomized trial of asymptomatic subjects, the perioperative risk of stroke and death was very low (1.5%), but the results indicated that a prohibitively high number of subjects (83) must be treated to prevent one stroke in 2 years. The subsequent literature reported higher perioperative risks (2.8% to 5.6%). In asymptomatic individuals nearly half of the strokes that occur may be due to heart and small-vessel disease. These limitations counter any potential benefit. Another trial is in progress and may identify subgroups of asymptomatic subjects who would benefit. Meanwhile, most individuals without symptoms fare better with medical care.The prevention of ischemic stroke by surgical means goes back half a century. After initial endorsement of carotid endarterectomy, confusion arose as to the appropriate selection of patients and the allowable risk from the procedure. In the past 2 decades large randomized trials have been used to evaluate the benefit of the procedure for patients with symptomatic and asymptomatic disease of the internal carotid artery. Sufficient time has now passed since the publication of these trials to analyze their impact on practice and to make recommendations about the application of carotid endarterectomy. There is strong evidence of benefit in some symptomatic patients, whereas other patients will not benefit and may even face harm. There is weak statistical and weaker clinical evidence that asymptomatic subjects will survive longer without experiencing stroke if they undergo endarterectomy than if they do not. The evidence supporting carotid angioplasty and stenting remains anecdotal and conflicting.The purpose of the present report is to provide a clinical roadmap to which symptomatic patients and asymptomatic subjects with carotid stenosis are candidates for endarterectomy. The risks and complications of endarterectomy are also reported. The outlook and benefit for symptomatic patients and asymptomatic subjects are so different that the evidence supporting appropriate use of endarterectomy in these 2 groups will be presented separately.     

Quantification of D-dimer and soluble fibrin in blood plasma of people with ischemic heart disease and hypertension

The method of D-dimer quantification in the human blood plasma has been developed using monoclonal antibodies 111-3b and II-4d. The method has been verified on the blood plasma of the patients with ischemic heart disease with and without stenocardia and with hypertension. The results showed that at ischemic heart disease with and without stenocardia and at hypertension the quantities of D-dimer in the blood plasma were generally less than the highest normal level 500 ng/ml (64.3%, 76.2% and 95%, correspondingly). The semiquantitative measurements of soluble fibrin levels in blood plasmas of the patients with ischemic heart disease and hypertension have been performed. It has been shown that the quantity of soluble fibrin at these diseases range greatly from < 0.03 mg/ml to 0.15 mg/ml. There was no correlation between the quantities of D-dimer and soluble fibrin in blood plasmas of the patients. Electrophoresis in PAAG with SDS showed that the soluble fibrin at these diseases had the mo- lecular mass of the fibrin (ogen). Thus the soluble fibrin in blood plasmas analysed consisted mainly of fibrin desAA oligomers (may be with fibrinogen incorporation) which are not stabilized by the factor XIIIa.     

Myocardial ischaemia in patients with frequent angina pectoris.

One hundred patients with angina pectoris underwent 16-point electrocardiographic (ECG) mapping of the left hemithorax during a standardised exercise test. Forty-five patients had maximum ST-segment depression at position V5, while 35 had no ECG signs of ischaemia at this position. In 20 V5 was on the edge of the precordial area, which showed less severe ST-depression than the central positions. An Oxford ECG recorder and highspeed analyser were modified and used in 50 of the patients with daily angina for recording ST-segment changes over 24 hours. Serial 24-hour ambulatory recordings from the edge of the precordial area of ischaemia identified during exercise detected a mean of only 14 +/- SD 3% of the episodes of ST-segment changes recorded from the centre of the same area. Only 16 +/- 2% of the episodes detected by ECG were accompanied by chest pain. More episodes occurred between 4 am and 6 am than at any other time during the night. This study shows the importance of recording ECG evidence of ischaemia from the precordial position showing maximum changes during exercise. ECG evidence of ischaemia occurs more frequently than anginal pain. These objective measurements add important information to the frequency of chest pain reported by patients with ischaemic heart disease.     

Insulin and Non-esterified Fatty Acid Metabolism in Asymptomatic Diabetics and Atherosclerotic Subjects

Glucose, insulin and non-esterified fatty acid (NEFA) metabolism was studied in 18 patients (mean age 49) with ischemic heart disease (IHD) who did not have any concurrent disorder known to affect glucose tolerance.Significant hyperglycemia and hyperinsulinemia were observed in the IHD patients after oral glucose. The serum NEFA declined to a lower level in IHD patients than in normal subjects who received glucose.In response to hypoglycemia following the oral administration of sodium tolbutamide the serum NEFA in IHD patients rose to a higher level in the rebound phase than in normal subjects. This rise was preceded by a sharp decline in the concentration of circulating insulin.In 72% of the patients (IHD sub-group) the blood glucose values after oral glucose satisfied the criteria for the diagnosis of diabetes mellitus. The metabolic changes following oral glucose in the IHD sub-group and in asymptomatic diabetics (AD), free of clinical atherosclerosis and with similar impairment in glucose tolerance, were compared. Despite insignificantly lower insulin concentrations, the AD showed a significantly lesser fall in circulating NEFA than did the patients in the IHD sub-group. After oral sodium tolbutamide the IHD sub-group patients showed a greater insulin response and a greater rebound increase in circulating NEFA than did the AD.These differences in response to oral glucose and to sodium tolbutamide suggest that the pathogenesis of the impaired glucose tolerance in IHD may be different from that responsible for abnormal carbohydrate tolerance in asymptomatic diabetics without evident atherosclerosis. The abnormalities demonstrated in glucose, insulin and NEFA metabolism may play a role in the genesis of the hyperlipoproteinemia and atherosclerosis of IHD. One possible mechanism leading to hyperlipoproteinemia in ischemic heart disease compatible with the data is discussed.     

Time of day and occurrence of myocardial ischemia]

A 24-hour Holter ECG was registered in 130 patients with the ischemic heart disease with or without the history of myocardial infarction treated in out-patient clinic. Two hundred thirty seven episodes of myocardial ischemia were detected. These episodes developed between 6.00 and 8.00 a.m., 12.00 and 4.00 p.m., and 6.00 and 8.00 p.m.     

Endoplasmic reticulum stress-induced hepatic stellate cell apoptosis through calcium-mediated JNK/P38 MAPK and Calpain/Caspase-12 pathways

Since ischemic heart disease (IHD) is a major cause of mortality and heart failure, novel therapeutic strategies are expected to improve the clinical outcomes of patients with acute myocardial infarction. Brief episodes of ischemia/reperfusion performed at the onset of reperfusion can reduce infarct size; a phenomenon termed “ischemic postconditioning.” Extensive research has determined that different autacoids (e.g., adenosine, bradykinin, opioid, etc.) and cytokines, their respective receptors, kinase signaling pathways, and mitochondrial modulation are involved in ischemic conditioning. Modification of these factors by pharmacological agents mimics the cardioprotection by ischemic postconditioning. Here, the potential mechanisms of ischemic postconditioning, the presence of comorbidities, and the possible extrapolation to the clinical setting are reviewed. In the near future, large, multicentered, randomized, placebo-controlled, clinical trials will be required to determine whether pharmacological and/or ischemic postconditioning can improve the clinical outcomes of patients with IHD.     

Prognosis of patients with "chest pain ?cause".

All 662 patients admitted to the two coronary care units in Nottingham during 12 consecutive months were followed up prospectively for one year. At the time of discharge from hospital they were categorised according to set criteria into the following diagnostic groups: definite, probable, or possible myocardial infarction; ischaemia heart disease without infarction; chest pain ?cause; and other diagnoses. Eighty-nine patients (13% of admissions) were categorised as having chest pain ?cause. No deaths occurred among these patients during the observation period, although two were readmitted with myocardial infarction. Patients with chest pain ?cause had few problems during the year after admission, and at the end of that time 75% were in their original employment. Patients admitted with ischaemic heart disease had a similar death rate (between six weeks and one year after admission) to those with myocardial infarction, and only 36% were in their original employment one year after admission. Chest pain ?cause is a clinically useful diagnostic category to which patients may be allocated after only simple investigations.     

Cytomegalovirus disease as a possible etiologic factor for early atherosclerosis

A group of 284 patients who underwent orthotopic heart transplantation between April 1986 to June 1991 and who were followed up for at least five years was analyzed in this paper. Patients were divided into three groups according to the presence or absence of cytomegalovirus infection or disease: patients without infection, patients with serologycaly proven infection and patients with cytomegalovirus disease. The analysis of survival was performed with respect to all major factors that influence survival: age and sex of a donor and a recipient, number of rejection episodes, perioperative ischemic time and pulmonary vascular resistence. A recipient's age was shown to be a significant factor. Patients who experienced at least one episode of cytomegalovirus disease had significantly worse long-term survival compared to those with the infection only or without the infection. That difference was caused by the increased incidence of coronary atherosclerosis, which caused deaths in patients with a previous episode of cytomegalovirus disease. A possible mechanism responsible for this phenomenon is discussed.     

Vascular Disease and Risk Stratification for Ischemic Stroke and All-Cause Death in Heart Failure Patients without Diagnosed Atrial Fibrillation: A Nationwide Cohort Study

Background

Stroke and mortality risk among heart failure patients previously diagnosed with different manifestations of vascular disease is poorly described. We conducted an observational study to evaluate the stroke and mortality risk among heart failure patients without diagnosed atrial fibrillation and with peripheral artery disease (PAD) or prior myocardial infarction (MI).

Methods

Population-based cohort study of patients diagnosed with incident heart failure during 2000–2012 and without atrial fibrillation, identified by record linkage between nationwide registries in Denmark. Hazard rate ratios of ischemic stroke and all-cause death after 1 year of follow-up were used to compare patients with either: a PAD diagnosis; a prior MI diagnosis; or no vascular disease.

Results

39,357 heart failure patients were included. When compared to heart failure patients with no vascular disease, PAD was associated with a higher 1-year rate of ischemic stroke (adjusted hazard rate ratio [HR]: 1.34, 95% confidence interval [CI]: 1.08–1.65) and all-cause death (adjusted HR: 1.47, 95% CI: 1.35–1.59), whereas prior MI was not (adjusted HR: 1.00, 95% CI: 0.86–1.15 and 0.94, 95% CI: 0.89–1.00, for ischemic stroke and all-cause death, respectively). When comparing patients with PAD to patients with prior MI, PAD was associated with a higher rate of both outcomes.

Conclusions

Among incident heart failure patients without diagnosed atrial fibrillation, a previous diagnosis of PAD was associated with a significantly higher rate of the ischemic stroke and all-cause death compared to patients with no vascular disease or prior MI. Prevention strategies may be particularly relevant among HF patients with PAD.     

Nonlinear Heart Rate Variability features for real-life stress detection. Case study: students under stress due to university examination

Background

Elevated transient ischemic ST segment episodes in the ambulatory electrocardiographic (AECG) records appear generally in patients with transmural ischemia (e. g. Prinzmetal's angina) while depressed ischemic episodes appear in patients with subendocardial ischemia (e. g. unstable or stable angina). Huge amount of AECG data necessitates automatic methods for analysis. We present an algorithm which determines type of transient ischemic episodes in the leads of records (elevations/depressions) and classifies AECG records according to type of ischemic heart disease (Prinzmetal's angina; coronary artery diseases excluding patients with Prinzmetal's angina; other heart diseases).

Methods

The algorithm was developed using 24-hour AECG records of the Long Term ST Database (LTST DB). The algorithm robustly generates ST segment level function in each AECG lead of the records, and tracks time varying non-ischemic ST segment changes such as slow drifts and axis shifts to construct the ST segment reference function. The ST segment reference function is then subtracted from the ST segment level function to obtain the ST segment deviation function. Using the third statistical moment of the histogram of the ST segment deviation function, the algorithm determines deflections of leads according to type of ischemic episodes present (elevations, depressions), and then classifies records according to type of ischemic heart disease.

Results

Using 74 records of the LTST DB (containing elevated or depressed ischemic episodes, mixed ischemic episodes, or no episodes), the algorithm correctly determined deflections of the majority of the leads of the records and correctly classified majority of the records with Prinzmetal's angina into the Prinzmetal's angina category (7 out of 8); majority of the records with other coronary artery diseases into the coronary artery diseases excluding patients with Prinzmetal's angina category (47 out of 55); and correctly classified one out of 11 records with other heart diseases into the other heart diseases category.

Conclusions

The developed algorithm is suitable for processing long AECG data, efficient, and correctly classified the majority of records of the LTST DB according to type of transient ischemic heart disease.     

An integrated study of heart pain and behavior in freely moving rats (using fos as a marker for neuronal activation)

The awareness in specific brain centers of angina pectoris most often results from ischemic episodes in the heart. These ischemic episodes induce the release of a collage of chemicals that activate chemosensitive and mechanoreceptive receptors in the heart, which in turn excite receptors of the sympathetic afferent pathways. Ascending pain signals from these fibers result in the activation of the brain centers which are involved in the perception and integration of cardiac pain. Cytochemical studies of the nervous system provide the opportunity to identify these areas at the cellular level. In the present investigation, cardiac nociception was studied in the brains and the spinal cords of rats, using Fos protein as a marker of neuronal activation, following the application of pain-inducing chemicals to the heart. Induction of myocardial pain in conscious rats was achieved by infusion of bradykinin (0.5 microg) or capsaicin (5 microg) into the pericardial sac. During pain stimulation, the rats demonstrated pain behavior, in conjunction with alterations in heart rate and blood pressure. The cerebral Fos expression pattern was studied 2 h after pain stimulation. In contrast to the control group, increased Fos expression was found following the use of both capsaicin and bradykinin in a variety of areas of the brain. Bradykinin, but not capsaicin, induced Fos expression in the upper thoracic and upper cervical spinal cord; these segments are the sites where cardiac sympathetic fibers terminate. This finding suggests that these two chemicals use two different pathways, and provides extra evidence for the role of the vagus nerve in the transmission of cardiac nociception. Different cerebral areas showed an increase in the c-fos activity following pericardial application of pain-inducing chemicals. The role of these cerebral areas in the integration of cardiac pain is discussed in relation to the identified pathways which transmit cardiac pain.     

131I]metaiodobenzylguanidine therapy of malignant pheochromocytoma: interference of medication

Malignant pheochromocytoma may present as a widespread metastatic disease, which is little or non-responsive to external beam radiotherapy and chemotherapy. The prognosis of these patients is bad due to both the progressive metastasis and the secretion of excess catecholamines which may cause hypertensive episodes. For these conditions [131I]metaiodobenzylguanidine (131I-MIBG) therapy may be an alternative treatment modality to induce both tumor remission and reduction of hormonal activity of the disease. The experience with 131I-MIBG therapy in four patients with metastatic malignant pheochromocytoma at The Netherlands Cancer Institute is reviewed. One patient with abdominal tumor recurrence and metastases to the lymph nodes and lungs had a partial remission of disease for 3 years; a second had a mixed response together with palliation and two other patients had stable disease, but were relieved of bone pain and severe hypertension, respectively. It is essential to be aware of the medication the patient is using, as many drugs are known or may be expected to interfere with the uptake and/or retention of 131I-MIBG by the tumor cells. The case of a significant reduction of 131I-MIBG uptake and retention by Labetalol in one of the patients is discussed. It is concluded that 131I-MIBG therapy may induce objective remission in patients with malignant pheochromocytoma and is certainly meaningful in the reduction of hormonal activity, the control of hypertension and the relief of pain from metastases.     

Immediate and long-term outcomes of the use of a Crossflex wire coronary stent in the treatment of patients with different forms of ischemic heart disease

Immediate and medium-term prognoses were studied in patients with coronary heart disease in whom a Crossflex wire coronary stent (Cordis, Johnson & Johnson, USA) had been inserted into the coronary arteries. The study indicated that it could be effectively used in patients with both chronic coronary heart disease and its exacerbation (acute myocardial infarction). It was found that in the vast majority of patients anginal attacks ceased and the clinical course ran smoothly in both immediate and medium-term postoperative periods. In the immediate period, various complications were observed only in 6.7% of cases. In the late period, the incidence of restenosis was 24%. If restenosis occurred, repeated balloon dilatation was successfully made in the great majority of cases by resulting in recovery of the vascular lumen.     

Exercise ECG changes in normal women

Submaximal and/or maximal exercise was carried out by 357 women without a history of cardiovascular disease, using a bicycle ergometer and/or treadmill while monitored by a bipolar ECG lead CM₅. In 40- to 60-year-old women the incidence of an ischemic ECG pattern during or after exercise ranged from 20 to 50%. Because clinical coronary disease can be expected in less than 10% of normal women followed for 16 years, most of these ECG changes were not considered to be due to occult coronary disease. At the present time exercise ECG changes in women cannot be used with any reliability as an aid in the diagnosis of chest pain or in screening normal female populations for coronary heart disease.     

Cerebral complications in juvenile rheumatoid arthritis.

The antecedents of myocardial infarction have been reviewed in 102 patients (117 episodes) undergoing a program of rehabilitation. The year prior to the first attack was characterized by business and social problems, with some weight gain; in the week before the attach there was added tiredness, poor general health and, in some cases, increasing anginal pain. Heavy lifting and/or unusual exercise were common immediately before or during an attack; five attacks were related to the shovelling of wet snow.Both bed and the normal place of work were uncommon sites for an attack. More than 50% of patients had 30 minutes'' warning of infarction. The relevance of these findings to a safe program of therapeutic exercise is discussed.     

Ischemic Colitis

Twenty cases of ischemic colitis are reviewed; 19 were obtained from autopsy files and the diagnosis in one was made from a surgical specimen. The majority of the patients were elderly with generalized arteriosclerosis. In approximately two-thirds of the patients the ischemic colitis was precipitated by preceding trauma, operation or congestive heart failure. Clinically, ischemic colitis is characterized by abdominal pain, distension and bleeding per rectum. Perforation of large bowel may occur. The lesions tend to be localized around the splenic flexure and junction of the descending and sigmoid colon, and in cases following aortic graft surgery the rectum is involved. Microscopically, there is necrosis, hemorrhage and ulceration. In less severe cases the mucosa only is affected. Cases with perforation show necrosis of all layers. It is considered that ischemic colitis is comparatively frequent and should be distinguished from other inflammatory conditions of the colon.