Lower gastrointestinal tract dysfunction in patients receiving long-term hemodialysis

Severe bowel dysfunction developed in 25 of 945 patients receiving long-term hemodialysis during a ten-year period. Colonic perforation occurred in 12 patients, six of whom died due to peritonitis. In seven instances, the perforation occurred spontaneously. Ten other individuals exhibited prolonged, severe adynamic ileus that progressed to colonic pseudo-obstruction in eight patients. Medical decompression (eight patients) and surgical bowel decompression (two patients) resulted in recovery in nine. Aluminum hydroxide gel, which was taken regularly by all patients, was associated with notable chronic constipation prior to the occurrence of bowel perforation or protracted adynamic ileus in 78% of these individuals.     

Anorexia nervosa with ischemic necrosis of the segmental ileum and cecum

A 41-year-old woman with long-standing anorexia nervosa showed paralytic ileus and serum creatine kinase elevation. Surgical treatment showed necrosis of the segmental ileum and cecum with perforation. She died of septic shock 3 days after the operation. Postmortem examination revealed no occlusion of the superior mesenteric artery or its main branches, and no arteriosclerotic changes. Histological examinations confirmed non-occlusive mesenteric infarction. This case suggested that necrosis of bowels might have been caused by poor blood supply due to severe malnutrition and dehydration for many years, which could be one of the fatal complications of anorexia nervosa.     

Heart wall rupture as a grave complication of acute myocardial infarct

The rupture of the heart wall is a severe complication of the acute myocardial infarction. We found it in 3.5% of the deceased patients with an acute myocardial infarction. The average age of these patients was 71 years. 75% of the patients died during the first five days after the event of the myocardial infarction. Apart from elderly patients with myocardial infarction such ones with a transmural myocardial infarction in the region of the left ventricle, an enlargement of the heart and signs of an insufficiency of the left heart, with a hypertension and diabetes mellitus seemed to be endangered. These patients need the most exact control and observation and in case of suspicion (symptomatology of angina pectoris which is continuing to exist) of a developing rupture of the heart wall and aimed diagnostics (echocardiography) and therapy must be begun immediately.     

Myocardial enzyme depletion in infarcted human hearts: infarct size and equivalent tissue mass

Myocardial activities of several enzymes were measured in infarcted and non-infarcted areas of heart sections obtained from eight patients who died after acute myocardial infarction. Similar data were obtained from four patients with cardiovascular disorders who died from causes other than myocardial infarction and from six patients without previously known heart disease. It was found that both non-infarcted and infarcted tissue samples contained considerably altered enzyme activities. This finding explains the low correlations between enzymatic and histological estimates of infarct size previously reported. However, when the residual myocardial activities of different enzymes were compared with each other, a close correlation was found between creatine kinase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase. It appears that the pathological changes in the myocardial activities of these enzymes may be explained by the phenomenon of diluted myocardium. This indicates that myocardial injury, as estimated from plasma enzyme activities, may still be expressed meaningfully in gram equivalents of healthy myocardium.     

Incidence of embolic or thrombotic processes during the immediate convalescence from acute myocardial infarction

One hundred consecutive cases of acute coronary occlusion and myocardial infarction were studied, and the incidence of subsequent intravascular thrombosis or embolism during the immediate convalescent period has been tabulated.Complications of a thrombotic or embolic nature occurred in thirty-seven cases. In four cases the complication caused the death of the patients, in eight cases the complications were contributing factors in the death of the patients, and in seventeen other cases the complication was of considerable importance in the future health of the persons concerned.A second myocardial infarction occurred in fifteen cases, pulmonary embolism occurred in fourteen cases, cerebral thrombosis or embolism complicated eight cases, arterial occlusions were noted in four instances, and thrombophlebitis complicated seven cases.Forty-six of the patients were known to have had normal blood pressure prior to the coronary occlusion and myocardial infarction. Ten (22 per cent) had subsequent myocardial infarctions during the immediate convalescent period. Forty-two of the total group of one hundred patients had had hypertension prior to coronary occlusion, and two (5 per cent) had subsequent myocardial infarctions during the immediate convalescent period. In twelve cases, the blood pressure prior to coronary occlusion was not definitely known. Three of these patients had a second myocardial infarction during their residence in the hospital.Eighty-seven per cent of the cases of second myocardial infarction and 87 per cent of the instances of cerebral vascular accidents occurred between the fourth and the twentieth day, and 86 per cent of the cases of thrombophlebitis occurred between the tenth and the sixteenth day, periods when the blood pressure of patients who have acute myocardial infarctions has been demonstrated to be at the lowest levels.Thirteen of the patients died. Two of them died as a result of cerebral thrombosis, one from pulmonary embolism, and one from a second myocardial infarction. Two other patients died of congestive heart failure. In seven instances death was sudden, but the exact cause was not ascertained.     

Excretion of myoglobin in urine after actue myocardial infarction.

We studied myoglobin excretion in 33 patients admitted to the coronary care unit with a provisional diagnosis of acute myocardial infarction. Sixteen proved to have definite and uncomplicated acute myocardial infarction and 17 possible infarction, using WHO criteria. For 5 days after admission, aliquots of every urine specimen voided by each patient were analysed for myoglobin using an immunochemical method able to detect a minimum urinary myoglobin concentration of 0-02 mg/ml. Myoglobinuria was detected in 14 of the 16 patients with definite infarction but was not found in any of the 17 patients with possible infarction. There were 3 patterns of myoglobin excretion. In 8 of the 14 patients it was excreted in one episode starting 10 to 40 hours after the onset of chest pain and lasting for 5 to 45 hours. In 3 of the remaining patients it was excreted over a much longer period (mean 83 hours) and in the final 3 patients myoglobinuria occurred in 2 or 3 intermittent episodes with periods of between 10 and 20 hours during which it was not detected. Total myoglobin excretion, which varied between 2 and 100 mg (mean 51 mg), did not correlate with peak serum enzyme levels. We concluded that in the appropriate clinical setting, the finding of myoglobinuria provides additional evidence for a diagnosis of acute myocardial infarction. The variable myoglobin excretion pattern suggests that in seemingly uncomplicated myocardial infarction there is considerable variation between patients in the pattern of evolution of the infarction process. This may be relevant to the assessment of measures directed towards limiting infarct size.     

Preventable deaths: who, how often, and why?

If the quality of care provided by a hospital affects its death rate, then some deaths must be preventable. We have developed a new method to investigate this issue and have reviewed 182 deaths from 12 hospitals (6 high outliers and 6 low outliers for death rate) for three conditions (cerebrovascular accident, pneumonia, or myocardial infarction). The investigators prepared a dictated summary of each patient's hospital course. Then, at least three physicians reviewed each summary and independently judged whether the death could have been prevented. Using a majority rules criterion (at least two of three physicians agreed), we found that 27% of the deaths might have been prevented. Using a unanimity criterion (all three physicians independently agreed), we found a 14% rate of probably preventable deaths. Patients whose deaths were probably preventable were younger (74.7 compared with 78.6 years, P less than 0.05), less often demented (12% compared with 26%, P less than 0.05), and less severely ill (mean Acute Physiology and Chronic Health Evaluation score, 15.6 compared with 21.2; P less than 0.001) than patients whose deaths were nonpreventable. The physicians also listed causes for each probably preventable death; nine reasons encompassed almost all of them. For myocardial infarction, preventable deaths reflected errors in management. For cerebrovascular accident, however, deaths primarily reflected errors in diagnosis. The severity of illness can help a hospital retrospectively identify probably preventable deaths. In the group of patients who died, 42% of those with a low severity of illness had probably preventable deaths as compared to 11% admitted with a high severity of illness. We found that a significant number of hospital deaths might have been prevented. Our findings were based on a new method that needs further testing to substantiate its validity. These findings also need replication before they can be generalized to other hospitals.     

Intra-aortic balloon pumping in coronary artery disease

Cardiogenic shock and severe left ventricular failure after acute myocardial infarction, refractory angina pectoris at rest either of new onset or superimposed on stable angina pectoris, or occurring in the post infarct (less than 2 weeks) period, and the suspicion of a slowly evolving infarction are the main indications for intra-aortic balloon pumping at the Thoraxcenter. 76 patients were treated with intra-aortic balloon pumping for cardiogenic shock after acute myocardial infarction and left ventricular failure, 42/76 (55%) could be weaned, 9 (12%) died within 3 months, 33 (43%) survived over 3 months, to date 29 are alive. 42 patients with refractory angina at rest were treated with intra-aortic balloon pumping. Pain relief was prompt in 41 (98%), who subsequently underwent coronary artery bypass grafting. Total myocardial infarction rate was 11% (5/42), total mortality rate was 7%. Perioperative myocardial infarction rate was 8% (4/42) and perioperative mortality was 7% (3/42). Pain relief was prompt in 14/17 patients (82%) with post infarct refractory angina. In 3 patients pain persisted despite intra-aortic balloon pumping, all sustained a myocardial infarction, 1 died, 2 other patients were excluded for surgery. 12 patients underwent coronary artery bypass grafting, none died, none developed acute myocardial infarction, 3 have mild stable angina. In 8 patients a slowly evolving myocardial infarction was suspected. Pain relief was prompt in 7/8 (88%) after institution of intra-aortic balloon pumping. Intra-aortic balloon pumping improves prognosis in cardiogenic shock after myocardial infarction, and abolishes refractory ischemic pain.     

Primary antiphospholipid syndrome as a cause of intestinal infarction.

We describe 2 patients with primary antiphospholipid syndrome who developed intestinal infarction. In one it was preceded by intestinal angina and, upon surgery, was found to have a hypertrophied media of mesenteric arteries. In the other, the intestinal infarction developed abruptly and was found to be due to mesenteric thrombosis. Arterial occlusions in primary antiphospholipid syndrome may involve the mesenteric arteries causing intestinal infarction. Some lesions may be proliferative and others thrombotic. Their clinical course may reflect this. Intestinal infarction seems to be part of the clinical spectrum of primary antiphospholipid syndrome.     

Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of acute myocardial infarction

Thrombolytic drugs given to patients with a mistaken diagnosis of acute myocardial infarction could produce adverse effects, although no such cases have been reported. Two patients treated with intravenous streptokinase for presumed but nonexistent acute myocardial infarction are described. Pericardial tamponade developed in both patients, in one after aortic dissection and in the other after pericarditis. Both required surgery; one died. Symptoms and electrocardiographic abnormalities mimicking acute myocardial infarction may be caused by non-coronary syndromes. In such cases, treatment with thrombolytic agents may exacerbate the underlying disease process and produce cardiovascular complications.     

Prediction of rupture in acute myocardial infarction

In two patient series including 809 and 327 patients, respectively, with acute myocardial infarction we have compared those who died in myocardial rupture (verified at autopsy, Group A) with those who died without rupture (autopsied, Group B), and those who survived hospitalization (Group C) with regard to previous history and clinical course in hospital. Rupture among autopsied patients was observed in 45% and 40% of the cases in the respective studies. Previous infarction was observed in each study as 0% and 0% in Group A compared with 25% and 31% in Group B, and 20% and 34% in Group C. Previous angina pectoris was observed in 26% and 22% in Group A compared with 50% and 54% in Group B and 52% and 54% in Group C. Maximum serum enzyme activity in Group A did not differ from Group B, but was higher than in Group C (p less than 0.001). Group A patients tended to have a higher initial pain score and a higher requirement of analgesics compared with other groups, whereas initial heart rate or systolic blood pressure did not differ in these patients compared to others. We thus conclude that patients with myocardial rupture have a very low occurrence of previous myocardial infarction and angina pectoris, and that their pain course appears to be particularly severe in the acute phase.     

Ischemic Heart Disease in the Elderly: A Need to Understand the Causes of High Mortality After Acute Myocardial Infarction

The short- and long-term mortality of patients >75 years of age with acute myocardial infarction is still very high. These patients have been excluded from most randomized controlled trials designed to test interventions directed to improve the outcome of acute myocardial infarction. Contrary to young-old patients (65–74 years) in whom the benefit obtained with these interventions is even greater than that observed in younger patients, there is a lack of information concerning the optimal treatment of acute myocardial infarction in the oldest patients. Research specifically directed to assess the optimal reperfusion strategy and coadjuvant therapies in patients >75 years old is critically important. The causes for such high mortality are still poorly understood. Several clinical observations suggest that old patients with acute myocardial infarction have specific pathophysiologic behaviors. As the knowledge of the mechanisms of disease is, in clinical practice, the basis of therapy development, clinical and basic research designed to elucidate the specific pathophysiological mechanisms and causes of the high mortality in the oldest patients with acute myocardial infarction should be regarded as a priority in geriatric cardiovascular research.     

Prognosis and Clinical Follow-Up of Patients Resuscitated from Out-of-Hospital Cardiac Arrest

ABSTRACT A new organization has been formed in which ambulance personnel have been trained to recognize ventricular tachycardia and ventricular fibrillation (VF) and to defibrillate. Cardiac arrest (CA) occurred in 307 patients and 140 were defibrillated. Twenty-eight patients were resuscitated and admitted for further hospital care. A previous history of ischaemic heart disease was found in 24 patients. Twenty-two of the patients admitted were found to have VF, two asystole and four other rhythms. All 11 survivors regained circulation at the site of the CA. At the time of admission all but one of the patients were unconscious and one longtime survivor remained unconscious until the 5th day following admission. Seventeen patients died while still in hospital. In 16 cases a diagnosis of acute myocardial infarction was established, a further six had VF without evidence of acute myocardial infarction and six had other diagnoses. Ten out of the 11 survivors were still alive six months after discharge. Only one case of recurrent VF was seen during a median follow-up period of 16 months. Prolonged coma, especially in combination with convulsions, was associated with a poor prognosis, while early return of circulation was significantly more common among survivors. Ongoing medication with β-blockers, a high QRS rate on admission and VF without proof of any acute myocardial infarction were also found to be more common in survivors.     

Rhythmusstörungen während der Remodelingphase nach Herzinfarkt

BACKGROUND: The effect of mechanical on electrical remodeling or electrical instability of the heart shows that it is essential for the prevention of sudden death to avoid or delay mechanical remodeling and neurohumoral activation after myocardial infarction. In other words, patients after myocardial infarction prone to neurohumoral activation need to be treated with ACE inhibitors or perhaps AT1-receptor blockers and beta blockers to maintain electrical stability. ICD INDICATION: MADIT I and MUSTT study showed that patients with severe ventricular dysfunction after myocardial infarction are at high risk of sudden death, especially in presence of electrical instabilities indicated by ventricular arrhythmias. These patients certainly need an automatic implantable cardioverter defibrillator (ICD). It is not clear so far whether or not the indication needs to be extended according to the MADIT II study. In other words, need all postmyocardial infarction patients with reduced pump function an ICD? There is no doubt that many patients with an ejection fraction below 30% have ventricular arrhythmias and fulfil therefore the inclusion criteria for the MADIT I or MUSTT study. In MADIT I, a run of three ventricular premature beats force was sufficient to fulfil the inclusion criteria. CONCLUSION: Another important consequence of the temporal correlation between mechanical and electrical remodeling is that specific attention must be directed to these interrelations in patients after myocardial infarction. Patients who die of sudden death show in comparison to surviving patients a substantial dilatation of the left ventricular during 6 months of observation which parallel the increasing incidence of ventricular premature beats. The consequence for therapy would be that in patients who present with left ventricular dilatation during 6 months after myocardial infarction, electrical instability is present and a high risk of sudden death exists. These patients probably will benefit from an ICD.     

Five cases of hematological disorders associated with acute myocardial infarction in thrombocytopenia]

Case of hematological disorders associated with acute myocardial infarction had been found in five of forty five autopsy cases which had hematological disorders during the past seven years. The five cases of hematological disorders consisted of two cases of myelodysplastic syndrome, a case of aplastic anemia, a case of primary myelofibrosis in blast transformation, and a case of acute myelogenous leukemia. All the patients were over 60 years old. Four patients had coronary artery stenosis and extensive myocardial infarction. Fibrinogen degradation products were elevated in four patients. DIC was recognized in two and suspected in two others. In all cases, platelet counts markedly decreased to less than 2.5 x 10(10)/L. Since no chest pain was noted by any patient, it was difficult to diagnose acute myocardial infarction without autopsy, except in one case. It is important to recognize the possibility of severe cardiac dysfunction due to myocardial infarction in thrombocytopenia, especially in the aged with DIC.     

Predictive value of plasma interleukin 1, interleukin 6, interleukin 8 and C-reactive protein (CRP) in patients with myocardial infarction

Long-term risk of mortality in patients with myocardial infarction is thought to be linked with plasma concentrations of proinflammatory cytokines and CRP (markers of inflammation). The aim of our study was to analyze plasma levels of interleukin (IL) 1, interleukin 6, interleukin 8 and C-reactive protein (CRP) in patients with myocardial infarction. One hundred and seven (107) patients with myocardial infarction hospitalized at the Cardiac Care Unit of St. Elizabeth's Sisters' Hospital in Warsaw and a control group of 10 subjects were enrolled in our study. The samples of peripheral venous blood were withdrawn from the patients on 2nd and 7th of infarction and plasma levels of IL-1, IL-6, IL-8 and CRP were determined. The patients were followed-up for a year. The analysis of survivals and deaths caused by acute coronary syndrome allowed to determine the predictive value of IL-1, IL-6, IL-8 and CRP in myocardial infarction. Twenty-two (22) of the total 107 patients died of acute coronary syndrome during one-year follow-up. Plasma IL-6 and CRP levels were higher in non-survivors as compared to the levels of IL-6 and CRP in living subjects, whereas plasma levels of IL-1 and IL-8 were comparable in both groups. IL-6 and CRP proved to be of predictive value in patients with myocardial infarction during one-year follow-up. It has also been found that plasma IL-6 level correlates with plasma CRP concentration and that there is a positive correlation between the former and CK-MB levels. IL-6 and CRP levels were higher in patients with Q wave infarction in comparison with non-Q wave infarction. Plasma levels of IL-1 and IL-8 have not been found to be good predictors of death during 12-month follow-up.     

Is there an ethnic difference in the prevalence of lupus cystitis? A report of six cases

Lupus cystitis was rare but frequently resulted in obstructive uropathy and had a strong association with gastrointestinal (GI) symptoms. We treated six patients with systemic lupus erythematosus (SLE) and obstructive uropathy from January 1996 to December 2001 in a university hospital. Evidence of cystitis was obtained from cystoscopic biopsy or the presence of thickened bladder wall in image study. Similar to other reports, five patients had GI manifestations such as abdominal pain, nausea/vomiting, diarrhoea or ileus. In addition, mesenteric lymphadenopathy or pancreatitis was noted in three patients. Two patients had been treated for idiopathic thrombocytopenic purpura (ITP), four and 20 years ago, respectively. All six patients had antibodies to double-stranded DNA (dsDNA). Five patients each had antibodies to cardiolipin (IgG aCL) or SSA. The high prevalence of anti-SSA had also been reported in Chinese lupus patients with intestinal pseudo-obstruction, a clinical manifestation frequently associated with bilateral ureterohydronephrosis. Two patients died of intractable infection after the surgical procedures for persistent ureterohydronephrosis and both patients had antibodies to ribosomal P proteins. Lupus cystitis might not be so rare in Chinese patients with SLE. The diagnosis should be kept in mind when lupus patients have urinary and/or GI symptoms.     

Myocardial consequences of coronary artery bypass graft surgery. The paradox of necrosis in areas of revascularization.

Myocardial infarction after coronary artery bypass graft (CABG) surgery has been described clinically in up to 30% of patients but there is little morphologic information about the character and pathogenesis of the myocardial injury. We studied myocardium in the distribution of bypassed and nonbypassed coronary arteries for the presence of contraction band necrosis as compared to coagulation necrosis, in 58 autopsied patients who died less than 1 month after surgery. Operation related necrosis consisting of focal subendocardial contraction band necrosis was present to some degree in 48 (83%) patients. Regional transmural necrosis was present in 22 (38%) patients and was of two types. Contraction band necrosis occurred in 18 patients and was in the distribution of a patent bypassed coronary artery in 15 of them. Coagulation necrosis was found in four patients, and in each was in the distribution of a new graft-releated coronary artery occlusion. The results suggest that coronary artery reflow through widely patent grafts following the period of operative nonperfusion, rather than graft or intrinsic coronary artery occlusion, accounts for the majority of operation-related myocardial "infarcts" associated with CABG surgery. Thus, prevention of intraoperative myocardial injury must also focus on characteristics of the phase of myocardial reperfusion.     

Complete heart block in acute myocardial infarction: drug therapy

A prospective investigation of medication in the treatment of complete heart block in acute myocardial infarction (AMI) was undertaken in the Coronary Care Unit of the Municipal Hospital, Copenhagen, during the period Nov. 24, 1967, to August 31, 1970.The material comprises 32 consecutive cases, corresponding to 8 per cent of all patients with verified acute myocardial infarction treated in the Unit during the same period. Treatment consisted in atropine, isoprenaline, and occasionally corticosteroids.Twelve patients died. In five the medication was without sufficient effect, and transvenous intracardial demand pacemakers were therefore employed. Three of these patients died. In the remaining nine fatal cases, sinus rhythm had been achieved in seven before death. The causes of death in these cases were: cardiac collapse, pulmonary embolism, or myocardial rupture. Two patients died after ventricular fibrillation.The mortality rate among the patients admitted in a state of cardiogenic shock was high, but with these exceptions it was not possible to predict the prognosis from the condition on admission.Eight out of 15 patients with infarctions of the anterior wall and 3 out of 16 patients with infarctions of the posterior wall died. The highest mortality rate was encountered in the combination of anterior wall infarction and a widened QRS complex.It cannot be ruled out that the chronotropic treatment may have resulted in an increased tendency to ectopic ventricular dysrhythmias, but this did not influence the mortality rate.The results obtained correspond to those observed in comparable materials using prophylactic pacemaker technique.It is concluded that by medication it is as a rule possible to achieve results similar to those of pacemaker therapy in complete heart block in acute myocardial infarction. However, pacemaker implantation may be life-saving in some cases and is indicated under all circumstances in Stokes-Adams attacks, persistent bradycardia with reduced cardiac output, and in repeated ventricular tachycardia during medication. In addition, prophylactic pacemaker implantation should be considered in anterior wall infarction with widened QRS complex, as this type of patient may frequently and suddenly develop complete heart block directly from sinus rhythm.     

Alterations in serum creatine kinase and lactate dehydrogenase. Association with abdominal aortic surgery, myocardial infarction and bowel necrosis

Experimental studies have shown that peripheral serum creatine kinase and lactate dehydrogenase change with bowel infarction. Some clinical reports have suggested that similar changes occur in patients. This prospective study documents the changes in these enzymes associated with acute myocardial infarction, acute bowel necrosis (MES INF), and uncomplicated abdominal aortic reconstruction. Analysis of 15 patients with AMI, 13 patients undergoing major AAS, and eight patients with MES INF has shown that these conditions may be differentiated by analysis of serum CK and LD isoenzymes. The study suggests that in the absence of electrocardiographic changes, a patient with epigastric distress with elevated levels of serum CK and either CK-MB or CK-BB bands present may well have a mesenteric rather than a myocardial infarction. Acute myocardial infarction can be ruled out further through analysis of serum LD1/LD2 ratios.