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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under the aspect of systemic diseases and their manifestation in the gut the following conclusions can be drawn: 1. The skin is the mirror of the intestinal tract; not only in primary gastroenterological disorders one should look for dermatological complications, but should also think in chronic skin lesions of concomitant intestinal alterations. 2. In all patients with collagen diseases a gastrointestinal involvement is very common. 3. In all endocrine disorders except in hypothyroidism diarrhea is a very common finding. 4. Infiltrations of gastrointestinal tract can be demonstrated in many cases by gastric, small bowel or rectal biopsy. 5. In all forms of dysgammaglobulinemia giardiasis is very common. 6. In right heart failure protein-losing enteropathy should be considered, in left ventricular insufficiency bowel ischemia.
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PMID:[Manifestations of systemic diseases in the gastrointestinal tract]. 96 97

The pulmonary artery of anesthetized dogs was constricted until right ventricular failure occurred (decreased cardiac output and aortic blood pressure; elevated right ventricular end-diastolic pressure). Coronary blood flow distribution was measured by means of an electromagnetic flowmeter and radioactive microspheres. With moderate levels of pulmonary stenosis (right ventricular pressure to 60 per cent of systemic pressure), right ventricular coronary flow increased (30 per cent, p smaller than 0.01) despite a significant fall in right ventricular driving pressure (aorto-right atrial pressure). Right ventricular failure occurred when right ventricular coronary flow did not increase sufficiently to meet raised oxygen requirements. Opening a pulmonary-systemic shunt during right ventricular failure increased pulmonary blood flow but lowered coronary driving pressure further, as blood was diverted into the lungs through the low-resistance fistula. Consequently, right ventricular coronary flow fell 50 per cent (p smaller than 0.01) and right ventricular failure with pulmonary stenosis resulted in a 362 per cent (p smaller than 0.01) increase in right coronary flow plus improved cardiac output. We made the following conclusions: (1) Right ventricular failure with pulmonary stenosis and intact ventricular septum is due to inadequate right ventricular blood flow to meet raised oxygen demands; (2) opening a pulmonary-systemic shunt may potentiate this failure and exaggerate ischemia by lowering coronary driving pressure and reducing right ventricular coronary flow.
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PMID:Effects of systemic-pulmonary shunts on regional myocardial blood flow in experimental pulmonary stenosis. 115 98

Right ventricular failure has been noted in up to 25% of patients requiring a left ventricular assist device. Altered septal motion or function is one proposed mechanism of right ventricular failure during left heart bypass. We studied the effect of regional ischemia and reperfusion of the interventricular septum on right ventricular function during complete left heart bypass. In six calves the septal perforating branches of the proximal left anterior descending coronary artery were isolated for intermittent occlusion. Complete left heart bypass was established with a Pierce-Donachy left ventricular assist device. Right and left ventricular function were studied with two-dimensional echocardiography and with intraventricular pressure monitors. Establishment of left heart bypass did not significantly affect right ventricular developed pressure, right ventricular end-diastolic area, or right ventricular fractional change in area. Left heart bypass significantly (p less than 0.001) decreased percent systolic septal wall thickening. Septal ischemia during left heart bypass resulted in a decrease in right ventricular developed pressure (p = 0.09), significant increase in right ventricular end-diastolic area (p = 0.002) and significant decrease in right ventricular fractional change in area (p less than 0.001), and a further decrease in interventricular septal wall thickening (p = 0.016). The interventricular septum became thin with flattening of its normal contour. Septal reperfusion resulted in right ventricular recovery with significant improvement in all factors (p less than 0.02). Similar results were documented during a second episode of septal ischemia with recovery after septal reperfusion. In some cases, septal ischemia may be an important factor in the development of right ventricular failure during left heart bypass.
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PMID:Ischemia of the interventricular septum. A mechanism of right ventricular failure during mechanical left ventricular assist. 159 84

Right ventricular infarction frequently occurs in the setting of infarction of the inferior wall of the left ventricle. Although there are several protective mechanisms that may limit the size of the infarction, right ventricular damage can result in right ventricular failure and cardiogenic shock. ECG manifestations of right ventricular infarction can facilitate the early recognition of this syndrome. The standard 12-lead ECG may provide some evidence of infarction of the right ventricle. ST-segment elevation in right precordial leads, however, is far more reliable in establishing a diagnosis. These leads should be recorded immediately if the standard 12-lead ECG reveals an acute inferior wall MI. Continuous ST-segment monitoring may be useful in the early detection of ongoing right ventricular ischemia. ECG markers can aid in the prompt institution of appropriate treatment. It is clear that early recognition of right ventricular infarction can have important diagnostic and therapeutic implications.
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PMID:Electrocardiographic considerations in right ventricular infarction. 159 53

In 1983, a previously healthy 21-year old mother came to University Hospital in Dijon, France feeling weak and had a severe frontal headache with vomiting. Clinical and biochemical tests were normal. She smoked 20 cigarettes/day and used a high dosed combined oral contraceptive (OC) (ethinyl estradiol and cyproterone acetate). 15 days later, the headache returned and she could not understand spoken words and the bilateral section of the brain had slowed. Yet her mental status was normal as were cerebrospinal fluid and cerebral computerized tomography tests. The antiherpes virus drug, vidabarine, did not alleviate symptoms. At least 1 month later, a severe left pulmonary embolism caused acute right heart failure. She also had a prethrombotic left iliac vein, so physicians began heparin therapy, adding nifedipine and buflomedil to control the spasms in the right internal iliac artery and both external iliac arteries. Acute ischemia of the lower limbs eased within a week but sensory disorders remained for 2 months. Satisfactory collaterality transpired due to a blocked left external iliac artery and left iliac vein. The following signs and symptoms indicated her condition to be homocystinuria: blond hair with deep blue eyes, macrocytic anemia, factor VII deficit (51%), strong positive Brandt's reaction, cystine homocystine in the plasma, and presence of homocystine, cystathionine, and methionine in the urine. Physicians took her off the OC and discharged her on vitamin B6/day, folic acid/day, betaine citrate/day, and the anticoagulant Coumadin. A subsequent check of her 19-year old sister found she had it too. They assessed the patient's condition yearly. In 1988, her left leg developed edema and she limped when not using elastic stockings. Effects of iliac vein phlebitis were evident. She no longer suffered from headaches. Since plasma methionine was within the normal range and homocystine no longer was present in plasma and urine, the physicians halted the anticoagulant therapy. In conclusion, the OC precipitated this partial form of homocystinuria.
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PMID:Vascular manifestations in homocystinuria. 161 Jun 63

To better understand the factors predisposing a patient to death after elective percutaneous transluminal coronary angioplasty (PTCA) and to gain insight into indications for high-risk PTCA both with and without adjunctive use of support devices, the outcomes of 8,052 consecutive procedures were reviewed. Death occurred after 32 procedures (0.4%) and was directly related to coronary artery closure in 26 (81%) of these cases. Left ventricular failure due to vessel closure at the dilated site, the most common cause of death, was independently correlated with female sex (p less than 0.001), "jeopardy score" (p less than 0.001) and PTCA of a proximal right coronary artery site (p = 0.002), but not with left ventricular ejection fraction or presence of multivessel disease. Right ventricular failure after closure of the proximal right coronary artery, and left main coronary dissection accounted for the majority of the remaining deaths. Systolic blood pressure immediately after coronary artery closure was also closely correlated with jeopardy score, and cardiogenic shock was frequent in women with scores greater than or equal to 3.5 and in men with scores greater than or equal to 5.0. These data highlight the superiority of the jeopardy score versus ejection fraction in the determination of risk, stress the importance of gender in determining outcome and point to the need for better means of right ventricular protection from severe ischemia. Therefore, an initial framework for rational use of PTCA and support devices in the high-risk setting is established.
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PMID:Causes and correlates of death after unsupported coronary angioplasty: implications for use of angioplasty and advanced support techniques in high-risk settings. 174 25

Systolic ventricular interactions may be partially responsible for right ventricular failure that sometimes occurs during clinical use of prosthetic left ventricular assist devices. In this hypothesis, it is proposed that the left ventricular assist device reduces left ventricular pressure and its contribution to right ventricular performance, thus impairing right ventricular output. On the other hand, these effects may be small compared with other causes of right ventricular failure such as ischemia. To test the systolic interaction hypothesis in the normal and ischemic right ventricle, we used a left ventricular assist device to pressure unload the left ventricle of anesthetized pigs, and we compared its effect on right heart function before and after 2 minutes of acute right coronary artery occlusion as a model of right heart failure. Pigs were instrumented for measurements of septal to left ventricular and right ventricular free wall dimensions with ultrasonic crystals, ventricular chamber pressures, and cardiac output with a pulmonary artery blood flow probe. Without right ventricular ischemia, the left ventricular assist device produced an 80% +/- 6% reduction in left ventricular pressure-time integral while maintaining aortic pressure. This resulted in a leftward septal shift with an 11.6% +/- 1.8% decrease in left ventricular septal-to-free wall dimension and a 12.5% +/- 2.4% increase in right ventricular septal-to-free wall dimension, with no changes in right ventricular cardiac output or stroke work. In contrast, right coronary artery occlusion alone produced right heart failure, with a 50% +/- 6% reduction in right ventricular global stroke work and 26% +/- 6% and 27% +/- 3% reductions in cardiac output and right ventricular peak systolic pressure, respectively. This right heart failure persisted during left ventricular unloading with the left ventricular assist device, which resulted in further leftward septal shifting and unchanged but still depressed stroke work and flow output. These findings support the hypothesis that a preexisting pathologic condition is the dominant factor in determining right ventricular function during prosthetic left ventricular support and that direct anatomic interactions play a minor role.
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PMID:Effects of acute right ventricular ischemia on ventricular interactions during prosthetic left ventricular support. 192 35

Pulmonary hypertension causes right ventricular ischemia and failure as a result of increased afterload combined with reduced coronary blood flow. Increasing coronary driving pressure by raising aortic pressure with phenylephrine has been shown to reverse right ventricular ischemia from pulmonary hypertension in animals. Since vasodilators often fail to reduce afterload, we tested whether raising the coronary driving pressure would improve right ventricular function in man. Ten patients with pulmonary hypertension had hemodynamics and right ventricular coronary driving pressure measured before and 10 minutes after a steady state was reached with a phenylephrine infusion titrated to raise aortic pressure by 25 percent. Phenylephrine caused a significant (p less than .01) increase in mean aortic pressure (84 to 108 mm Hg) and right ventricular coronary driving pressure (46 to 69 mm Hg). In response, there was a significant (p less than .01) rise in mean pulmonary artery pressure (58 to 67 mm Hg), right ventricular end-diastolic pressure (10 to 16 mm Hg) and wedge pressure (5 to 9 mm Hg), and an insignificant fall in cardiac output (3.26 to 3.09 L/min) and pulmonary artery O2 saturation (57 to 49 percent). Although phenylephrine increased right ventricular coronary driving pressure, it worsened right ventricular function as manifest by a rise in end-diastolic pressure and fall in cardiac output. Any benefit of raising right ventricular coronary driving pressure may have been offset by alpha vasoconstriction of right ventricular coronary blood flow and/or pulmonary arterial vasoconstriction. Phenylephrine does not appear to be a useful therapy of right ventricular failure from pulmonary hypertension in patients who fail vasodilators.
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PMID:The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension. 198 87

A right ventricular assist device (VAD) based on the principle of counterpulsation has been developed at our institution. The device is a valveless, pneumatically actuated, 40 cc, sac-type pump, with a single inlet-outlet port. For right ventricular support, the "Uniport" pump is anastamosed end-to-side to the pulmonary artery. In previous experimental trials, the device has been shown to impart minimal trauma to blood components. In this study, biventricular failure was induced in eight Holstein calves by normothermic ischemia during cardiopulmonary bypass. A Pierce-Donachy left VAD (LVAD) was used for left ventricular support following the ischemic insult. Hemodynamic measurements were obtained throughout the study, and each animal served as its own control. A significant increase in post injury cardiac output (33.5 +/- 11.4%) was obtained with use of the Uniport and LVAD, as compared to use of the LVAD alone (p less than or equal to 0.005). Other hemodynamic parameters of right heart failure, including right atrial pressure (RAP), pulmonary artery pressure (PAP), and left atrial pressure (LAP) were not significantly affected. These data suggest that the Uniport right ventricular assist device significantly improves cardiac output in this model of moderate right ventricular failure. Additional studies are required, however, to optimize pump stroke volume, and to further define the performance envelope of the device.
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PMID:Hemodynamic effects of a new right ventricular assist device. 225 37

Right heart failure (RHF) during left heart bypass (LHB) has been recognized clinically. Two hypotheses concerning RHF during LHB exist: one suggests that the cause is related to LHB itself, and another suggests that RHF existed prior to LHB. By using 16 mongrel dogs, the influence of LHB and ventricular septal ischemia on the right heart was studied experimentally. Under the extracorporeal circulation the coronary septal branch was dissected and a suture was hooked around the artery for the ligation. To maintain a constant right ventricular (RV) preload at 100 ml/kg/min, blood was drained from both the superior and inferior venae cavae, and was sent to the right atrium (RA) by a roller pump. Functional parameters of right heart, such as RA pressure, RV pressure, the first derivative of RV (RV dp/dt) and RV free wall contractile width, were measured while the LHB between left atrium and femoral artery was established. The measurements were done before and after the ligation of the septal branch, and were also done during LHB when the LHB ratio was changed from 0, 40, 60, 80, 100, 100, 80, 60, 40 and 0% of RV preload. RV free wall contractile width, measured by ultrasonic method, and the Max RV dp/dt were decreased significantly when LHB ratio was increased and both were increased when LHB ratio was decreased. When the septal branch was ligated, the contractile width was decreased significantly. The max RV dp/dt was also decreased but not significantly. When the LHB was performed after ventricular septal branch ligation, the trend of the RV functional changes was similar to that before ligation.
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PMID:[Experimental study on right ventricular function during left heart bypass--in a coronary septal branch ligation model]. 234 94


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