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Results for “Recovery phases”

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PubMed1991

Transplantation with blood stem cells.

Peripheral blood stem cell transplantation (PBSCT) offers an alternative to autologous bone marrow transplants (A-BMT), especially in malignant diseases with bone marrow contamination. The presence of hemopoietic precursors in peripheral blood has been documented in several animal models and in humans. While many of these precursors might be committed cells with finite renewal capacity, ample evidence suggests that true pluripotent stem cells are circulating in a number sufficient to enable sustained trilineage engraftment after transplantation. Stem cell mobilization is markedly increased in the early recovery phase after intensive chemotherapy and can be promoted by the administration of various cytokines or polyanionic substances. These effects are used to optimize stem cell harvesting by leukapheresis. Clinical trials of PBSCT have been performed in several hundred patients with various hematological and nonhematological malignancies. Recovery was generally more rapid than after A-BMT. However, the envisioned advantage concerning disease control has not been documented so far.

Hematopoietic Stem Cell Transplantation↗

PubMed1998

The effect of gammadelta T cell depletion on cytokine gene expression in experimental allergic encephalomyelitis.

In experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, we showed previously that depletion of gammadelta T cells using the mAb GL3 immediately before disease onset, or during the chronic phase, significantly ameliorated clinical severity. We now report on the effect of gammadelta T cell depletion on expression of five cytokine genes, IL-1, IL-6, TNF, lymphotoxin, and IFN-gamma in spinal cords of mice during the pre-onset, onset, height, and recovery phases of EAE, and on expression of type II nitric oxide synthase. In control animals, the mRNAs for IL-1 and IL-6 rose dramatically at disease onset and peaked before disease height, whereas the mRNAs for TNF, lymphotoxin, and IFN-gamma rose more slowly and peaked with peak of disease. In GL3-treated animals, a dramatic reduction in all five cytokines was noted at disease onset, but only IFN-gamma remained significantly reduced at a time point equivalent to height of disease in control animals. ELISA data confirmed the reduced levels of IL-1 and IL-6 at disease onset in GL3-treated animals, and pathologic analysis demonstrated a marked reduction in meningeal infiltrates at the same time point. Studies of type II NOS also demonstrated a significant reduction in both mRNA and protein expression at the height of disease in GL3-treated animals. These results suggest that gammadelta T cells contribute to the pathogenesis of EAE by regulating the influx of inflammatory cells into the spinal cord and by augmenting the proinflammatory cytokine profile of the inflammatory infiltrates.

Animals↗

PubMed1995

Functional brain organization in bipolar affective patients during manic phase and after recovery: a digit dichotic listening study.

To study the functional organization of the cerebral hemispheres in patients with bipolar psychosis using a verbal dichotic listening test for pairs of digits 26 patients were tested twice, during the acute expression of manic phase and after recovery. The patient group during the manic phase did not support the expected right-ear advantage of normal subjects on verbal dichotic tests but showed a statistically significant left-ear advantage, which shifted after recovery toward the typical normal asymmetry. Comparing patients during the manic phase and after recovery showed that the left-ear advantage as well as the shift in right-ear advantage after recovery was due to the reduction of left-ear performance. From the over-all neuropsychological findings for these patients mania may be hypothesized to be characterized by overactivation of the right hemisphere. This phaenomenon seems associated with acuteness of the symptoms of the psychotic disorder.

Acute Disease↗

PubMed2002

Serum and urinary insulin-like growth factor-1 and tumor necrosis factor in neonates with and without acute renal failure.

Acute renal failure (ARF) in neonates may occur after renal ischemia. Growth factors participate in the tubular regeneration process. Insulin-like growth factor-1 (IGF-1) is produced in the kidney during the recovery phase of ARF. Tumor necrosis factor-alpha (TNFalpha) may play a role in renal apoptosis. We examined serum and urinary IGF-1 and TNFalpha in neonates with or without ARF after asphyxia, in order to assess their possible use as markers of renal damage and recovery. We studied 20 full-term asphyxiated neonates, 10 with ARF and 10 without ARF, and compared them with 13 normal newborns for 7 days after birth. Blood urea, creatinine, pH, base deficit, and serum and urine IGF-1 and TNFalpha were assessed. Neonates with ARF had more-severe acidosis than patients without ARF. All patients had lower serum IGF-1 values immediately after birth than control children. Serum IGF-1 remained low in the ARF patients. The initial urinary IGF-1 was higher in all patients compared with control newborns, and remained elevated for the rest of the study only in the ARF neonates. Serum and urinary TNFalpha concentrations were similar for all healthy and diseased neonates. Measurement of serum and urinary IGF-1 levels in ARF neonates might be of additional value for clinical assessment of ARF.

Acute Kidney Injury↗

PubMed1991

Activated T lymphocyte subsets in experimental allergic neuritis.

Changes in activated T cell subsets in peripheral blood were examined during the course of experimental allergic neuritis (EAN), using two-color immunofluorescence flow cytometry. Both CD4+ and CD8+ activated T cells decreased transiently before the onset of clinical signs, and increased just around the time of onset of the disease. In contrast, during the recovery phase, the numbers of CD4+ activated T cells returned to the normal range, whereas CD8+ activated T cells continued to increase. These findings imply that activation of CD4+ helper/inducer cells contributes mainly to the evolution of EAN, and that of CD8+ suppressor cells are necessary for recovery.

Animals↗

PubMed2001

Intracellular pH regulation in colonocytes of rat proximal colon.

The regulation of intracellular pH (pH(i)) in colonocytes of the rat proximal colon has been investigated using the pH-sensitive dye BCECF and compared with the regulation of pH(i) in the colonocytes of the distal colon. The proximal colonocytes in a HEPES-buffered solution had pH(i)=7.24+/-0.04 and removal of extracellular Na(+) lowered pH(i) by 0.24 pH units. Acid-loaded colonocytes by an NH(3)/NH(4)(+) prepulse exhibited a spontaneous recovery that was partially Na(+)-dependent and could be inhibited by ethylisopropylamiloride (EIPA). The Na(+)-dependent recovery rate was enhanced by increasing the extracellular Na(+) concentration and was further stimulated by aldosterone. In an Na(+)- and K(+)-free HEPES-buffered solution, the recovery rate from the acid load was significantly stimulated by addition of K(+) and this K(+)-dependent recovery was partially blocked by ouabain. The intrinsic buffer capacity of proximal colonocytes at physiological pH(i) exhibited a nearly 2-fold higher value than in distal colonocytes. Butyrate induced immediate colonocyte acidification that was smaller in proximal than in distal colonocytes. This acidification was followed by a recovery phase that was both EIPA-sensitive and -insensitive and was similar in both groups of colonocytes. In a HCO(3)(-)/CO(2)-containing solution, pH(i) of the proximal colonocytes was 7.20+/-0.04. Removal of external Cl(-) caused alkalinization that was inhibited by DIDS. The recovery from an alkaline load induced by removal of HCO(3)(-)/CO(2) from the medium was Cl(-)-dependent, Na(+)-independent and blocked by DIDS. Recovery from an acid load in EIPA-containing Na(+)-free HCO(3)(-)/CO(2)-containing solution was accelerated by addition of Na(+). Removal of Cl(-) inhibited the effect of Na(+). In summary, the freshly isolated proximal colonocytes of rats express Na(+)/H(+) exchanger, H(+)/K(+) exchanger ((H(+)-K(+))-ATPase) and Na(+)-dependent Cl(-)/HCO(3)(-) exchanger that contribute to acid extrusion and Na(+)-independent Cl(-)/HCO(3)(-) exchanger contributing to alkali extrusion. All of these are likely involved in the regulation of pH(i) in vivo. Proximal colonocytes are able to maintain a more stable pH(i) than distal cells, which seems to be facilitated by their higher intrinsic buffer capacity.

Ammonium Chloride↗

PubMed2000

Ketamine anesthesia at high altitude.

There is a clinical need for a safe and effective anesthetic technique in high altitude and remote areas. This report presents a series of 11 consecutive cases documenting the use of ketamine anesthesia in a remote hospital at an altitude of 3,900 m, by primary-care physicians without specialist training in anesthesia. The method of administration is fully described. At a low dose of 2.0 mg/kg, ketamine produces a dissociative anesthesia that does not depress the hypoxic drive, or interfere with the pharyngeal or laryngeal reflexes. Although supplemental oxygen is useful in the recovery phase for less acclimatized individuals, it is usually not required as reductions in oxygen saturation can be raised by physical stimulation that encourages the patient to breathe faster and deeper. The common side effect of emergent nightmares was avoided using midazolam as premedication and a quiet recovery area. This study offers the first available evidence that ketamine with midazolam offers a safe and effective means of anaesthesia at very high altitude, without the need for specialist equipment or training, by careful clinicians experienced in basic airway management.

Acclimatization↗

PubMed2000

Optimal level of pressure support ventilation for recovery from diaphragmatic fatigue in rabbits.

OBJECTIVE: To determine whether there is an optimal level of pressure support ventilation (PSV) for recovery from acute diaphragmatic fatigue. DESIGN: Prospective laboratory trial. SETTING: Experimental laboratory. SUBJECTS: Twenty healthy adult New Zealand White rabbits. INTERVENTIONS: Diaphragmatic fatigue was induced with 50 Hz of phrenic nerve stimulation for 30 mins. Recovery was compared between inspiratory load + PSV of 0 cm H2O (L0), inspiratory load + PSV of 60 cm H2O (L60), inspiratory load + PSV of 80 cm H2O (L80), and PSV of 0 cm H2O without inspiratory load (SB) for 90 mins immediately after the end of the fatigue-inducing procedure. To add inspiratory load during the recovery phase, three pressure threshold valves, each having an opening pressure of -20 cm H2O, were used. MEASUREMENTS AND MAIN RESULTS: After the fatigue-inducing procedure, diaphragmatic electromyogram and transdiaphragmatic pressure remained at baseline in both SB and L60, decreased in L80, and increased in L0. Recovery was assessed by abdominal cavity pressure (Pabd) generated by high-frequency (100 Hz) and low-frequency (20 Hz) stimulation. Pabd at 100 Hz recovered to baseline in L60 and SB but not in L0 and L80 (69.1%, 81.3%, 100.3%, and 100.7% of the baseline at 90 mins for L0, L80, L60, and SB, respectively). Pabd at 20 Hz did not differ among ventilatory settings. CONCLUSION: There is an optimal range of PSV assist level to improve recovery from diaphragmatic fatigue. Recovery was hampered not only by inadequate PSV but also by excessive PSV.

Airway Resistance↗

PubMed2000

Lactate, glucose and O2 uptake in human brain during recovery from maximal exercise.

The metabolic activity of the brain has not been evaluated during physical exercise. In six volunteers substrate uptake by the brain was determined during graded exercise and recovery from maximal exercise by measuring the arterial-internal jugular venous concentration differences(a-v differences). The a-v difference for lactate increased from 0.02 +/- 0.08 mmol l-1 at rest to 0.39 +/- 0. 13 mmol l-1 during exercise and remained positive during 30 min of recovery (P < 0.05). The a-v difference for glucose (0.55 +/- 0.06 mmol l-1 at rest) did not change significantly during exercise, but during the initial 5 min of recovery it increased to 0.83 +/- 0.10 mmol l-1 (P < 0.05). The O2 a-v difference at rest of 3.11 +/- 0.30 mmol l-1 remained stable during exercise, then increased during the initial 5 min of recovery (3.77 +/- 0.52 mmol l-1) and remained high during the subsequent 30 min recovery period (3.62 +/- 0.64 mmol l-1; P < 0.05). Thus the O2/glucose uptake ratio did not change during exercise (pre-exercise 5.95 +/- 0.68; post-exercise 6.02 +/- 1.39) but decreased to 4.93 +/- 0.99 during the initial 5 min of recovery (P < 0.05). When lactate uptake was included, the resting O2/carbohydrate uptake ratio of 5.84 +/- 0.73 was reduced to 4.42 +/- 0.25 during exercise and decreased further during the recovery phase (to 3.79 +/- 0.30; P < 0.05). In contrast, in the resting and immobilised rat, lactate infusion to a level similar to that obtained during maximal exercise in humans did not affect the a-v difference for lactate. The large carbohydrate uptake by the brain during recovery from maximal exercise suggests that brain glycogen metabolism is important in the transition from rest to exercise, since this would explain the significant post-exercise decrease in the O2/carbohydrate uptake ratio.

Adult↗

PubMed1991

Abnormal vascular responses to supine exercise in hypertrophic cardiomyopathy.

BACKGROUND: Exercise hypotension has been documented in hypertrophic cardiomyopathy. It is not the result of an inability to augment cardiac output but instead relates to an inappropriate and exaggerated decrease in systemic vascular resistance at high work loads. METHODS AND RESULTS: To enable us to examine the behavior of the peripheral vasculature during exercise, 103 consecutive patients underwent maximal symptom-limited supine bicycle exercise with measurement of forearm blood flow. A minimum reduction of 12% from the basal value was defined as a normal response based on the study of 25 normal controls. In the patients, two patterns of forearm blood flow were observed. Sixty-four patients had an appropriate reduction in forearm blood flow of 40 +/- 16% from resting flow. In 39 patients, the forearm blood flow either failed to decrease or increased with exercise by 45 +/- 105% of the resting value. Patients with an abnormal forearm vasodilator response were younger (31 +/- 13 versus 46 +/- 14 years), and more of them had a family history of hypertrophic cardiomyopathy and sudden death than did those with a normal vasoconstrictor response (16 of 39 versus eight of 64). Left ventricular end-diastolic cavity dimensions were smaller in those with an abnormal forearm blood flow response, but other clinical, echocardiographic, and arrhythmic variables were similar. To assess the relation of abnormal peripheral vascular responses to erect exercise blood pressure response, patients underwent treadmill exercise testing with careful monitoring of systolic blood pressure response. Thirty-eight patients had significant exercise hypotension with failure of the systolic blood pressure to increase during progressive exercise (n = 6) or an abrupt decrease in systolic blood pressure (20-60 mm Hg) from the peak value (n = 32); 65 patients had a normal exercise blood pressure response, but 18 of these patients had an oscillation in systolic blood pressure of 10 mm Hg or more early in the recovery phase. Thirty-one of 39 patients with an abnormal forearm blood flow response demonstrated exercise hypotension during the erect exercise testing, and the remaining eight patients had a normal exercise blood pressure response; however, five of these eight had abnormal oscillations in blood pressure during recovery (r = 0.61, p less than 0.001). CONCLUSIONS: The relation of abnormal peripheral vascular responses to exercise hypotension confirms the observation of hemodynamic instability in patients with hypertrophic cardiomyopathy. The finding of abnormal vascular responses in patients known to be at increased risk (young age and a family history of hypertrophic cardiomyopathy and sudden death) suggests that hemodynamic mechanisms may be important in the occurrence of sudden death in hypertrophic cardiomyopathy.

Adolescent↗

PubMed2006

Brain pH response to hyperventilation in panic disorder: preliminary evidence for altered acid-base regulation.

OBJECTIVE: Previous findings of excess brain lactate and delayed end-tidal CO(2) (pCO(2)) recovery in subjects with panic disorder during hyperventilation suggested altered acid-base regulation. Two models were posited to explain these results: 1) subjects with panic disorder demonstrate greater alkalosis to hyperventilation, implicating increased lactate as directly compensatory, or 2) subjects with panic disorder demonstrate reduced or blunted alkalosis, implicating increased lactate as overly compensatory to a normal pH response. In both models, delayed pCO(2) recovery in subjects with panic disorder could reflect slower pH normalization in the recovery phase. METHOD: Asymptomatic medicated patients with panic disorder were studied during regulated hyperventilation. Phosphorous spectroscopy was used to measure brain pH every 2 minutes. Nine subjects with panic disorder were compared to 11 healthy subjects at baseline (five scans), during regulated hyperventilation (five scans), and across recovery (10 scans). Anxiety symptoms were assessed with standard ratings. RESULTS: No subject had a panic attack before hyperventilation. Subjects with panic disorder had lower pCO(2) during hyperventilation and slower pCO(2) recovery across the posthyperventilation interval. Despite this different respiratory response in the panic disorder group, brain pH increases were not significantly greater during hyperventilation, nor was pH return to baseline slowed during posthyperventilation. A linear regression model derived from data of healthy subjects showed pH blunting in the panic disorder group. CONCLUSIONS: Although subjects with panic disorder had greater hypocapnea during hyperventilation, their observed pH response, not altered from comparison levels, implicated exaggerated buffering. It is suggested that increased lactate could account for these findings.

Acid-Base Imbalance↗

PubMed2000

Tracking the recovery of local optic nerve function after optic neuritis: a multifocal VEP study.

PURPOSE: To explore the multifocal visual evoked potential (mVEP) as a technique for tracking local optic nerve damage after unilateral optic neuritis (ON). METHODS: Humphrey visual fields and mVEP recordings were obtained from three patients within 7 days of an episode of ON. Patients were retested during the recovery phase, approximately 4 to 7 weeks later. The multi-input procedure of Sutter was used to obtain 60 local VEP responses (the mVEP) to a scaled checkerboard pattern. The mVEPs were recorded separately for monocular stimulation of both eyes. RESULTS: Initially, all three patients had extensive visual field defects, reduced visual acuity, and depressed mVEP amplitude in regions of poor visual field sensitivity. By 4 to 7 weeks, the fields recovered to near normal sensitivity in most locations, and visual acuity returned to 20/20. The mVEP recovered to nearly full amplitude in all regions, but substantial delays were present in many locations. The delayed responses were associated with regions of visual field loss documented during the acute phase. CONCLUSIONS: The mVEP can be used to track local optic nerve damage after unilateral ON. This technique should be useful in observing the effects of treatments as well as in testing hypotheses about the mechanisms underlying both the acute loss of vision and the subsequent recovery.

Acute Disease↗

PubMed2004

Hematopoietic stem cells.

The hematopoietic system of the young child acquires, through time, the ability to cope with exposure to a number of environmental toxins and infectious agents. Occasionally, severe aplastic anemia occurs secondary to exposure to some of these toxins or infectious agents. The occurrence of severe aplastic anemia provides an opportunity to study the maturation of the hematopoietic system because often the immune system is partially intact. Hematopoietic stem cell transplants permit the study of the complete reconstitution of the hematopoietic and immunologic system. Stem cell transplants are often used to treat severe aplastic anemia or, alternatively, may be part of the treatment for an underlying malignant disease or a genetic disease. Sources of stem cells and the age of the recipient and donor have an impact on the success of the stem cell transplant. A stem cell transplantation provides a window of opportunity to study and observe the normal maturation of the immune system and the sensitivity. Very clearly, children recover from severe aplastic anemia and stem cell transplantations more readily with fewer problems and complications than adults. The environmental risks that a child who received a stem cell transplantation faces are related primarily to the deficiencies of the hematopoietic system and immune system during the recovery phase. Therefore, diminished resistance to infectious agents, primarily viruses and other opportunistic organisms, are the primary risk that children who are recovering from these transplantations face. There are few data on the susceptibility of these children to the toxic effects of other environmental toxicants during the recovery period, which may take years before complete recovery.

Anemia, Aplastic↗

PubMed2006

Further investigation of the mechanism of Doxorubicin release from P105 micelles using kinetic models.

The kinetics of the release of Doxorubicin from Pluronic P105 micelles during ultrasonication and its subsequent re-encapsulation upon cessation of insonation were investigated. Four mechanisms are proposed to explain the acoustically-triggered Doxorubicin (Dox) release and re-encapsulation from Pluronic P105 micelles. The four mechanisms are: micelle destruction; destruction of cavitating nuclei; reassembly of micelles, and the re-encapsulation of Dox. The first mechanism, the destruction of micelles during insonation, causes the release of Dox into solution. The micelles are destroyed because of cavitation events produced by collapsing nuclei, or bubbles in the insonated solution. The second mechanism, the slow destruction of cavitating nuclei, results in a slow partial recovery phase, when a small amount of Dox is re-encapsulated. The third and fourth mechanisms, the reassembly of micelles and the re-encapsulatin of Dox, are independent of ultrasound. These two mechanism are responsible for maintaining the drug release at a partial level, and for recovery after insonation ceases. A normal distribution was used to describe micellar size. Parameters for the model were determined based upon the best observed fit to experimental data. The resulting model provides a good approximation to experimental data for the release of Dox from Pluronic P105 micelles.

Doxorubicin↗

PubMed1997

A new model of renal microvascular endothelial injury.

Although the importance of injury with consequent activation of endothelium is well-recognized in diseases affecting the glomerular endothelial cell (GEN), research on GEN injury in vivo has been hampered by the lack of adequate animal models. Here we report the establishment and characterization of a new GEN injury model in rats. This model was induced by selective renal artery perfusion with anti-GEN IgG and resulted in the severe acute renal failure with marked platelet deposition and development of a thrombotic microangiopathy involving glomeruli. Peritubular capillary endothelial cells were also damaged that was associated with severe tubular necrosis. Although the glomerular changes were severe, half of the glomeruli recovered by day 10, while interstitial changes remained throughout our observation time course. Proliferation of GEN was observed during the recovery phase. An increased expression of endothelial nitric oxide synthase in GEN was also observed, and may be an adaptive mechanism to counteract the thrombosis and ischemia. This model should be useful to investigate the pathophysiology of renal microvascular diseases and the mechanisms of GEN injury, activation and recovery in vivo.

Acute Kidney Injury↗

PubMed1982

Suprathreshold vision in acute optic neuritis.

The perception of contrast was measured in patients with acute unilateral optic neuritis by a technique of subjective suprathreshold contrast matching, and was compared with contrast sensitivity as defined by threshold measurements. The suprathreshold apparent contrast and threshold contrast sensitivity was repeatedly assessed during the recovery phase. Generally, an attenuation of suprathreshold apparent contrast was found for high and intermediate spatial frequencies in the eye with optic neuritis. At a low spatial frequency, however, the suprathreshold contrast vision was spared. The threshold contrast sensitivity was not however, spared at low spatial frequencies. During recovery this frequency-specific loss in suprathreshold apparent contrast diminished and finally a "normal" suprathreshold contrast vision was observed in all affected eyes reaching a visual acuity of 1.0 or better. In these cases also subjectively normal vision was reported in site of a persisting abnormality in threshold contrast sensitivity.

Acute Disease↗

PubMed1985

Photoperiodic control of meiosis in the male Syrian hamster (Mesocricetus auratus).

Male Syrian hamsters exposed to short photoperiods of 6 h light/day (6L:18D) show regression of the testes within 12 weeks. Chromosome preparations of the meiotic stages (pachytene, metaphase I (MI) and metaphase II (MII)), testicular weights relative to body weights, sperm counts, seminiferous tubule diameter and histological appearance were examined at intervals during regression and subsequent recovery in a long photoperiod (14L:10D). The fall of testicular weight was associated with the decrease in tubule diameter. Spermatogenesis and sperm count were reduced rapidly and finally ceased after 10 weeks in short days. The numbers of MI and MII cells relative to 100 pachytene cells progressively decreased during the short-day treatment, although the ratio of MI:MII stayed constant whenever there was meiotic activity (except in the first week of the recovery phase). This suggests that an increasing proportion of pachytene cells did not progress to MI with increased time in short days, but cells which did reach MI progressed to MII in the same proportions as in the control testes. Meiosis ceased after 10 weeks in short days. Recovery in the long days was marked by a peak in the number of MI and MII cells/100 pachytene cells soon after the return to long days. This preceded the return (to control values) of the sperm count by 10 weeks. Initial recovery in the first 3 weeks was very rapid in all the determined values.

Animals↗

PubMedDate not supplied

Plasma CRP level predicts left ventricular function and exercise capacity in patients with acute myocardial infarction.

BACKGROUND: C-reactive protein estimation can help in predicting short- and long-term prognosis after acute myocardial infarction. High plasma C-reactive protein level in the acute phase strongly indicates a poor clinical outcome of the patients with myocardial infarction. METHODS AND RESULTS: One hundred consecutive patients admitted with ST elevation myocardial infarction in the intensive coronary care unit in our hospital who were able to do symptom-limited treadmill test during early recovery phase were studied. Plasma C-reactive protein was measured at the time of admission by immunoturbidity method. The normal value of the C-reactive protein was taken as 0.8 mg/dl. Echocardiographic study was done on day three of admission and ejection fraction was estimated by modified Simpson's method. Symptom-limited treadmill exercise test was done in all the patients. Patients were classified into two groups based on level of C-reactive protein: those with low C-reactive protein level (1.26 +/- 0.91 mg/dl, n=40) and those with high C-reactive protein level (6.52 +/- 3.97 mg/dl, n=60). Ejection fraction was lower in high C-reactive protein group (46.7 +/- 11.9%) compared to low C-reactive protein group (56.9 +/- 7.7%) (p = 0.011). Exercise capacity was lower in high C-reactive protein group (2.8 +/- 1.4 METs) compared to low C-reactive protein group (5.5 +/- 2.5 METs) p = 0.027). CONCLUSIONS: C-reactive protein levels are an index of the severity of myocardial necrosis which translate to worse left ventricular function. Higher the C-reactive protein level, lower the ejection fraction and worse may be the prognosis.

C-Reactive Protein↗