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International Journal of Environmental... Apr 2020Creatine monohydrate is a nutritional supplement often consumed by athletes in anaerobic sports. Creatine is naturally found in most meat products; therefore,...
BACKGROUND
Creatine monohydrate is a nutritional supplement often consumed by athletes in anaerobic sports. Creatine is naturally found in most meat products; therefore, vegetarians have reduced creatine stores and may benefit from supplementation.
OBJECTIVE
to determine the effects of creatine supplementation on vegetarians.
DATA SOURCES
PubMed and SPORTDiscus. Eligibility criteria: Randomized controlled trials (parallel group, cross-over studies) or prospective studies.
PARTICIPANTS
Vegetarians.
INTERVENTION
Creatine supplementation. Study appraisal and synthesis: A total of 64 records were identified, and eleven full-text articles (covering nine studies) were included in this systematic review.
RESULTS
Creatine supplementation in vegetarians increased total creatine, creatine, and phosphocreatine concentrations in vastus lateralis and gastrocnemius muscle, plasma, and red blood cells, often to levels greater than omnivores. Creatine supplementation had no effect on brain levels of phosphocreatine. Creatine supplementation increased lean tissue mass, type II fiber area, insulin-like growth factor-1, muscular strength, muscular endurance, Wingate mean power output, and brain function (memory and intelligence) in vegetarian participants. Studies were mixed on whether creatine supplementation improved exercise performance in vegetarians to a greater extent compared to omnivores.
LIMITATIONS
Studies that were reviewed had moderate-high risk of bias.
CONCLUSIONS
Overall, it appears vegetarian athletes are likely to benefit from creatine supplementation.
Topics: Athletes; Cognition; Creatine; Diet, Vegetarian; Dietary Supplements; Humans; Memory; Physical Fitness; Prospective Studies; Vegetarians
PubMed: 32349356
DOI: 10.3390/ijerph17093041 -
Journal of Vascular Surgery Oct 2017Intermittent claudication (IC) is frequently associated with deterioration in walking capacity and physical function, and it can often result in an impairment in... (Review)
Review
OBJECTIVE
Intermittent claudication (IC) is frequently associated with deterioration in walking capacity and physical function, and it can often result in an impairment in balance. Whereas supervised exercise is recommended by the National Institute for Health and Care Excellence as the first-line treatment, the mechanism behind walking improvement is poorly understood. The existing literature suggests that there may be some physiologic change to the skeletal muscle contributing to the functional impairment, but these data are conflicting. We therefore sought to undertake a systematic review to clarify the muscle properties of patients with IC.
METHODS
A systematic review of randomized and nonrandomized trials that investigated the role of muscle function in patients diagnosed with IC was undertaken using MEDLINE, Cochrane Central Register of Controlled Trials, and Embase databases. The searches were limited from 1947 to June 2016 in the English language.
RESULTS
The search yielded a total of 506 articles, of which 206 were duplicate articles. Of the remaining 300, a total of 201 were excluded from full-text analysis; 99 full-text articles were assessed for eligibility, with 30 articles deemed appropriate for inclusion in the review. There were four main categories of functional outcome measures: muscle strength, muscle size, muscle fiber type, and muscle metabolism. A total of 2837 patients were included in the study. Nine studies reported on muscle strength, incorporating isometric, concentric, eccentric, and endurance measures. Eight studies reported on muscle size, incorporating circumference, computed tomography scans, and ultrasound imaging techniques. Eleven studies reported on muscle fibers, incorporating fiber type proportions, fiber size, and capillarity measures. Seven papers reported on muscle metabolism, incorporating adenosine diphosphate recovery and phosphocreatine recovery measures.
CONCLUSIONS
Previous literature has found clear evidence that strength (of the calf and thigh musculature) and calf characteristics are related to mortality and functional declines. However, this review has demonstrated the vast array of muscle groups assessed and multiple methods employed to determine strength; therefore, it is unclear exactly what measure of "strength" is impaired. Furthermore, the underlying morphologic causes of potential changes in strength are unclear. This information is essential for designing optimal exercise interventions. The data acquired during this systematic review are heterogeneous, with a substantial lack of high-quality intervention-based studies. Future research should endeavor to establish standardized testing procedures and to implement randomized controlled trials for targeted therapeutic interventions.
Topics: Aged; Angioplasty; Exercise Therapy; Exercise Tolerance; Female; Humans; Intermittent Claudication; Lower Extremity; Male; Middle Aged; Muscle Strength; Muscle, Skeletal; Peripheral Arterial Disease; Recovery of Function; Treatment Outcome; Walking
PubMed: 28822657
DOI: 10.1016/j.jvs.2017.05.106 -
BMC Cancer May 2015The benefits associated with some cancer treatments do not come without risk. A serious side effect of some common cancer treatments is cardiotoxicity. Increased... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The benefits associated with some cancer treatments do not come without risk. A serious side effect of some common cancer treatments is cardiotoxicity. Increased recognition of the public health implications of cancer treatment-induced cardiotoxicity has resulted in a proliferation of systematic reviews in this field to guide practice. Quality appraisal of these reviews is likely to limit the influence of biased conclusions from systematic reviews that have used poor methodology related to clinical decision-making. The aim of this meta-review is to appraise and synthesise evidence from only high quality systematic reviews focused on the prevention, detection or management of cancer treatment-induced cardiotoxicity.
METHODS
Using Cochrane methodology, we searched databases, citations and hand-searched bibliographies. Two reviewers independently appraised reviews and extracted findings. A total of 18 high quality systematic reviews were subsequently analysed, 67 % (n = 12) of these comprised meta-analyses.
RESULTS
One systematic review concluded that there is insufficient evidence regarding the utility of cardiac biomarkers for the detection of cardiotoxicity. The following strategies might reduce the risk of cardiotoxicity: 1) The concomitant administration of dexrazoxane with anthracylines; 2) The avoidance of anthracyclines where possible; 3) The continuous administration of anthracyclines (>6 h) rather than bolus dosing; and 4) The administration of anthracycline derivatives such as epirubicin or liposomal-encapsulated doxorubicin instead of doxorubicin. In terms of management, one review focused on medical interventions for treating anthracycline-induced cardiotoxicity during or after treatment of childhood cancer. Neither intervention (enalapril and phosphocreatine) was associated with statistically significant improvement in ejection fraction or mortality.
CONCLUSION
This review highlights the lack of high level evidence to guide clinical decision-making with respect to the detection and management of cancer treatment-associated cardiotoxicity. There is more evidence with respect to the prevention of this adverse effect of cancer treatment. This evidence, however, only applies to anthracycline-based chemotherapy in a predominantly adult population. There is no high-level evidence to guide clinical decision-making regarding the prevention, detection or management of radiation-induced cardiotoxicity.
Topics: Animals; Anthracyclines; Antibiotics, Antineoplastic; Cardiotoxicity; Databases, Bibliographic; Disease Management; Humans; Neoplasms
PubMed: 25948399
DOI: 10.1186/s12885-015-1407-6 -
The Cochrane Database of Systematic... Dec 2014Creatine is an amino acid derivative and, when phosphorylated (phosphocreatine), is involved in replenishing adenosine triphosphate (ATP) via the creatine kinase... (Review)
Review
BACKGROUND
Creatine is an amino acid derivative and, when phosphorylated (phosphocreatine), is involved in replenishing adenosine triphosphate (ATP) via the creatine kinase reaction. Cells obtain creatine from a diet rich in fish, meat, or dairy and by endogenous synthesis from the amino acids arginine, glycine, and methionine in an approximate 50:50 ratio. Animal studies have shown that creatine may provide fetal neuroprotection when given to the mother through her diet in pregnancy. It is important to assess whether maternally administered creatine in human pregnancy (at times of known, suspected, or potential fetal compromise) may offer neuroprotection to the fetus and may accordingly reduce the risk of adverse neurodevelopmental outcomes, such as cerebral palsy and associated impairments and disabilities arising from fetal brain injury.
OBJECTIVES
To assess the effects of creatine when used for neuroprotection of the fetus.
SEARCH METHODS
We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (30 November 2014).
SELECTION CRITERIA
We planned to include all published, unpublished, and ongoing randomised trials and quasi-randomised trials. We planned to include studies reported as abstracts only as well as full-text manuscripts. Trials using a cross-over or cluster-randomised design were not eligible for inclusion.We planned to include trials comparing creatine given to women in pregnancy for fetal neuroprotection (regardless of the route, timing, dose, or duration of administration) with placebo, no treatment, or with an alternative agent aimed at providing fetal neuroprotection. We also planned to include comparisons of different regimens for administration of creatine.
DATA COLLECTION AND ANALYSIS
We identified no completed or ongoing randomised controlled trials.
MAIN RESULTS
We found no randomised controlled trials for inclusion in this review.
AUTHORS' CONCLUSIONS
As we did not identify any randomised controlled trials for inclusion in this review, we are unable to comment on implications for practice. Although evidence from animal studies has supported a fetal neuroprotective role for creatine when administered to the mother during pregnancy, no trials assessing creatine in pregnant women for fetal neuroprotection have been published to date. If creatine is established as safe for the mother and her fetus, research efforts should first be directed towards randomised trials comparing creatine with either no intervention (ideally using a placebo), or with alternative agents aimed at providing fetal neuroprotection (including magnesium sulphate for the very preterm infant). If appropriate, these trials should then be followed by studies comparing different creatine regimens (dosage and duration of exposure). Such trials should be high quality and adequately powered to evaluate maternal and infant short and longer-term outcomes (including neurodevelopmental disabilities such as cerebral palsy), and should consider utilisation/costs of health care.
Topics: Brain Diseases; Creatine; Female; Fetal Diseases; Humans; Neuroprotective Agents; Pregnancy
PubMed: 25523279
DOI: 10.1002/14651858.CD010846.pub2 -
Frontiers in Aging Neuroscience 2023Many lines of evidence suggest that mitochondria have a central role in aging-related neurodegenerative diseases, such as Alzheimer's disease (AD). Mitochondrial...
Many lines of evidence suggest that mitochondria have a central role in aging-related neurodegenerative diseases, such as Alzheimer's disease (AD). Mitochondrial dysfunction, cerebral energy dysmetabolism and oxidative damage increase with age, and are early event in AD pathophysiology and may precede amyloid beta (Aβ) plaques. probes of mitochondrial function and energy metabolism are therefore crucial to characterize the bioenergetic abnormalities underlying AD risk, and their relationship to pathophysiology and cognition. A majority of the research conducted in humans have used F-fluoro-deoxygluose (FDG) PET to image cerebral glucose metabolism (CMRglc), but key information regarding oxidative phosphorylation (OXPHOS), the process which generates 90% of the energy for the brain, cannot be assessed with this method. Thus, there is a crucial need for imaging tools to measure mitochondrial processes and OXPHOS in the human brain. Phosphorus-magnetic resonance spectroscopy (P-MRS) is a non-invasive method which allows for the measurement of OXPHOS-related high-energy phosphates (HEP), including phosphocreatine (PCr), adenosine triphosphate (ATP), and inorganic phosphate (Pi), in addition to potential of hydrogen (pH), as well as components of phospholipid metabolism, such as phosphomonoesters (PMEs) and phosphodiesters (PDEs). Herein, we provide a systematic review of the existing literature utilizing the P-MRS methodology during the normal aging process and in patients with mild cognitive impairment (MCI) and AD, with an additional focus on individuals at risk for AD. We discuss the strengths and limitations of the technique, in addition to considering future directions toward validating the use of P-MRS measures as biomarkers for the early detection of AD.
PubMed: 37273652
DOI: 10.3389/fnagi.2023.1183228 -
Applied Bionics and Biomechanics 2022The prognosis of mitral valve replacement is an important clinical issue and may produce unexpected mortality rates if not properly addressed. The postoperative...
PURPOSE
The prognosis of mitral valve replacement is an important clinical issue and may produce unexpected mortality rates if not properly addressed. The postoperative examination results have important prognostic implications. This study was designed to determine the prognostic value of phosphocreatine and inflammatory markers after mitral valve replacement.
METHOD
Comparison and analysis of the data obtained using SPSS software. The computer retrieved PubMed, Science Citation Index (SCI), Embase, VIP, CNKI, CBM, and Wanfang database and manually retrieved randomized controlled trials (RCTs) published at home and abroad on the central muscle protection role of creatine phosphate in heart valve replacement, and the search period was established until February 2018. Two random literature reviewers independently screened the literature and extracted data, using Review Manager (RevMan) (Computer program), version 5.3 (The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen, 2014). RevMan software version 5.0 assesses the risk of bias for inclusion in studies. The software performs a meta-analysis of the obtained data.
RESULTS
Ten RCTs with a total of 464 participants were enrolled. The meta-analysis results showed that (1) elevated creatine kinase levels often predict a better prognosis after mitral valve replacement (RR = 1.36, 95% CI: 1.22 to 1.52, < 0.00001), (2) the creatine kinase isoenzyme level in the venous blood of the phosphocreatine group after 24 h of aortic blocking was significantly lower than that in the control group (SMD = -2.90, 95% CI: -5.19 to -0.60, = 0.01), and (3) Troponin I levels were significantly lower in the intravenous creatine group than in the control group 24 h after opening of the aortic block (SMD = -1.49, 95% CI: -2.02 to -0.97, < 0.00001).
CONCLUSIONS
Creatine phosphate and inflammatory factor have good predictive value for the prognosis of mitral valve replacement.
PubMed: 35310686
DOI: 10.1155/2022/1132452 -
Journal of Clinical Medicine Oct 2023Exercise therapy as part of the clinical management of patients with neuromuscular diseases (NMDs) is complicated by the limited insights into its efficacy. There is an... (Review)
Review
Exercise therapy as part of the clinical management of patients with neuromuscular diseases (NMDs) is complicated by the limited insights into its efficacy. There is an urgent need for sensitive and non-invasive quantitative muscle biomarkers to monitor the effects of exercise training. Therefore, the objective of this systematic review was to critically appraise and summarize the current evidence for the sensitivity of quantitative, non-invasive biomarkers, based on imaging and electrophysiological techniques, for measuring the effects of physical exercise training. We identified a wide variety of biomarkers, including imaging techniques, i.e., magnetic resonance imaging (MRI) and ultrasound, surface electromyography (sEMG), magnetic resonance spectroscopy (MRS), and near-infrared spectroscopy (NIRS). Imaging biomarkers, such as muscle maximum area and muscle thickness, and EMG biomarkers, such as compound muscle action potential (CMAP) amplitude, detected significant changes in muscle morphology and neural adaptations following resistance training. MRS and NIRS biomarkers, such as initial phosphocreatine recovery rate (V), mitochondrial capacity (Q), adenosine phosphate recovery half-time (ADP t), and micromolar changes in deoxygenated hemoglobin and myoglobin concentrations (Δ[deoxy(Hb + Mb)]), detected significant adaptations in oxidative metabolism after endurance training. We also identified biomarkers whose clinical relevance has not yet been assessed due to lack of sufficient study.
PubMed: 37959299
DOI: 10.3390/jcm12216834 -
PloS One 2013Creatine kinase plays a key role in cellular energy transport. The enzyme transfers high-energy phosphoryl groups from mitochondria to subcellular sites of ATP... (Review)
Review
BACKGROUND
Creatine kinase plays a key role in cellular energy transport. The enzyme transfers high-energy phosphoryl groups from mitochondria to subcellular sites of ATP hydrolysis, where it buffers ADP concentration by catalyzing the reversible transfer of the high-energy phosphate moiety (P) between creatine and ADP. Cellular creatine uptake is competitively inhibited by beta-guanidinopropionic acid. This substance is marked as safe for human use, but the effects are unclear. Therefore, we systematically reviewed the effect of beta-guanidinopropionic acid on energy metabolism and function of tissues with high energy demands.
METHODS
We performed a systematic review and searched the electronic databases Pubmed, EMBASE, the Cochrane Library, and LILACS from their inception through March 2011. Furthermore, we searched the internet and explored references from textbooks and reviews.
RESULTS
After applying the inclusion criteria, we retrieved 131 publications, mainly considering the effect of chronic oral administration of beta-guanidinopropionic acid (0.5 to 3.5%) on skeletal muscle, the cardiovascular system, and brain tissue in animals. Beta-guanidinopropionic acid decreased intracellular creatine and phosphocreatine in all tissues studied. In skeletal muscle, this effect induced a shift from glycolytic to oxidative metabolism, increased cellular glucose uptake and increased fatigue tolerance. In heart tissue this shift to mitochondrial metabolism was less pronounced. Myocardial contractility was modestly reduced, including a decreased ventricular developed pressure, albeit with unchanged cardiac output. In brain tissue adaptations in energy metabolism resulted in enhanced ATP stability and survival during hypoxia.
CONCLUSION
Chronic beta-guanidinopropionic acid increases fatigue tolerance of skeletal muscle and survival during ischaemia in animal studies, with modestly reduced myocardial contractility. Because it is marked as safe for human use, there is a need for human data.
Topics: Administration, Oral; Animals; Brain; Cardiovascular System; Creatine Kinase; Energy Metabolism; Guanidines; Humans; Muscle, Skeletal; Propionates
PubMed: 23326362
DOI: 10.1371/journal.pone.0052879 -
The Cochrane Database of Systematic... Aug 2016Anthracyclines are frequently used chemotherapeutic agents for childhood cancer that can cause cardiotoxicity during and after treatment. Although several medical... (Review)
Review
BACKGROUND
Anthracyclines are frequently used chemotherapeutic agents for childhood cancer that can cause cardiotoxicity during and after treatment. Although several medical interventions in adults with symptomatic or asymptomatic cardiac dysfunction due to other causes are beneficial, it is not known if the same treatments are effective for childhood cancer patients and survivors with anthracycline-induced cardiotoxicity. This review is an update of a previously published Cochrane review.
OBJECTIVES
To compare the effect of medical interventions on anthracycline-induced cardiotoxicity in childhood cancer patients or survivors with the effect of placebo, other medical interventions, or no treatment.
SEARCH METHODS
We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (the Cochrane Library, 2015, Issue 8), MEDLINE/PubMed (1949 to September 2015), and EMBASE/Ovid (1980 to September 2015) for potentially relevant articles. In addition, we searched reference lists of relevant articles, conference proceedings of the International Society for Paediatric Oncology (SIOP), the American Society of Clinical Oncology (ASCO), the American Society of Hematology (ASH), the International Conference on Long-Term Complications of Treatment of Children & Adolescents for Cancer, and the European Symposium on Late Complications from Childhood Cancer (from 2005 to 2015), and ongoing trial databases (the ISRCTN Register, the National Institutes of Health (NIH) Register, and the trials register of the World Health Organization (WHO); all searched in September 2015).
SELECTION CRITERIA
Randomised controlled trials (RCTs) or controlled clinical trials (CCTs) comparing the effectiveness of medical interventions to treat anthracycline-induced cardiotoxicity with either placebo, other medical interventions, or no treatment.
DATA COLLECTION AND ANALYSIS
Two review authors independently performed the study selection. One review author performed the data extraction and 'Risk of bias' assessments, which another review author checked. We performed analyses according to the guidelines in the Cochrane Handbook for Systematic Reviews of Interventions.
MAIN RESULTS
In the original version of the review we identified two RCTs; in this update we identified no additional studies. One trial (135 participants) compared enalapril with placebo in childhood cancer survivors with asymptomatic anthracycline-induced cardiac dysfunction. The other trial (68 participants) compared a two-week treatment of phosphocreatine with a control treatment (vitamin C, adenosine triphosphate, vitamin E, oral coenzyme Q10) in leukaemia patients with anthracycline-induced cardiotoxicity. Both studies had methodological limitations.The RCT on enalapril showed no statistically significant differences in overall survival, mortality due to heart failure, development of clinical heart failure, and quality of life between treatment and control groups. A post-hoc analysis showed a decrease (that is improvement) in one measure of cardiac function (left ventricular end-systolic wall stress (LVESWS): -8.62% change) compared with placebo (+1.66% change) in the first year of treatment (P = 0.036), but not afterwards. Participants treated with enalapril had a higher risk of dizziness or hypotension (risk ratio 7.17, 95% confidence interval 1.71 to 30.17) and fatigue (Fisher's exact test, P = 0.013).The RCT on phosphocreatine found no differences in overall survival, mortality due to heart failure, echocardiographic cardiac function, and adverse events between treatment and control groups.
AUTHORS' CONCLUSIONS
Only one trial evaluated the effect of enalapril in childhood cancer survivors with asymptomatic cardiac dysfunction. Although there is some evidence that enalapril temporarily improves one parameter of cardiac function (LVESWS), it is unclear whether it improves clinical outcomes. Enalapril was associated with a higher risk of dizziness or hypotension and fatigue. Clinicians should weigh the possible benefits with the known side effects of enalapril in childhood cancer survivors with asymptomatic anthracycline-induced cardiotoxicity.Only one trial evaluated the effect of phosphocreatine in childhood cancer patients with anthracycline-induced cardiotoxicity. Limited data with a high risk of bias showed no significant difference between phosphocreatine and control treatments on echocardiographic function and clinical outcomes.We did not identify any RCTs or CCTs studying other medical interventions for symptomatic or asymptomatic cardiotoxicity in childhood cancer patients or survivors.High-quality studies should be performed.
Topics: Adult; Adult Survivors of Child Adverse Events; Angiotensin-Converting Enzyme Inhibitors; Anthracyclines; Antibiotics, Antineoplastic; Cardiotonic Agents; Child; Enalapril; Heart Failure; Humans; Neoplasms; Phosphocreatine; Randomized Controlled Trials as Topic
PubMed: 27552363
DOI: 10.1002/14651858.CD008011.pub3 -
The Cochrane Database of Systematic... Nov 2011The creatine kinase system, the central regulatory system of cellular energy metabolism, provides ATP in situ at ATP-ases involved in ion transport and muscle... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The creatine kinase system, the central regulatory system of cellular energy metabolism, provides ATP in situ at ATP-ases involved in ion transport and muscle contraction. Furthermore, the enzyme system provides relative protection from tissue ischaemia and acidosis. The system could therefore be a target for pharmacologic intervention.
OBJECTIVES
To systematically evaluate evidence regarding the effectiveness of interventions directly targeting the creatine kinase system as compared to placebo control in adult patients with essential hypertension or cardiovascular disease.
SEARCH METHODS
Electronic databases searched: Medline (1950 - Feb 2011), Embase (up to Feb 2011), the Cochrane Controlled Trials Register (issue 3, Aug 2009), Latin-American/Caribbean databank Lilacs; references from textbooks and reviews; contact with experts and pharmaceutical companies; and searching the Internet. There was no language restriction.
SELECTION CRITERIA
Randomized controlled trials comparing creatine, creatine phosphate, or cyclocreatine (any route, dose or duration of treatment) with placebo; in adult patients with essential hypertension, heart failure, or myocardial infarction. We did not include papers on the short-term use of creatine during cardiac surgery.
DATA COLLECTION AND ANALYSIS
The outcomes assessed were death, total myocardial infarction (fatal or non-fatal), hospitalizations for congestive heart failure, change in ejection fraction, and changes in diastolic and systolic blood pressure in mm Hg or as percent change.
MAIN RESULTS
Full reports or abstracts from 1164 papers were reviewed, yielding 11 trials considering treatment with creatine or creatine analogues in 1474 patients with heart failure, ischemic heart disease or myocardial infarction. No trial in patients with hypertension was identified. Eleven trials (1474 patients, 35 years or older) comparing add-on therapy of the creatine-based drug on standard treatment to placebo control in patients with heart failure (6 trials in 1226 / 1474 patients ), or acute myocardial infarction (4 trials in 220 / 1474 patients) or 1 in ischemic heart disease (28 / 1474 patients) were identified. The drugs used were either creatine, creatine phosphate (orally, intravenously, or intramuscular) or phosphocreatinine. In the trials considering heart failure all three different compounds were studied; creatine orally (Gordon 1995, Kuethe 2006), creatine phosphate via intravenous infusion (Ferraro 1996, Grazioli 1992), and phosphocreatinine orally (Carmenini 1994, Maggi 1990). In contrast, the acute myocardial infarction trials studied intravenous creatine phosphate only. In the ischemic heart disease trial (Pedone 1984) creatine phosphate was given twice daily through an intramuscular injection to outpatients and through an intravenous infusion to inpatients. The duration of the study intervention was shorter for the acute patients, from a two hour intravenous infusion of creatine phosphate in acute myocardial infarction (Ruda 1988, Samarenko 1987), to six months in patients with heart failure on oral phosphocreatinine therapy (Carmenini 1994). In the acute myocardial infarction patients the follow-up period varied from the acute treatment period (Ruda 1988) to 28 days after start of the symptoms (Samarenko 1987) or end of the hospitalization period (Zochowski 1994). In the other trials there was no follow-up after discontinuation of treatment, except for Gordon 1995 which followed the patients until four days after stopping the intervention.Only two out of four trials in patients with acute myocardial infarction reported mortality outcomes, with no significant effect of creatine or creatine analogues (RR 0.73, CI: 0.22 - 2.45). In addition, there was no significance on the progression of myocardial infarction or improvement on ejection fraction. The main effect of the interventions seems to be on improvement of dysrhythmia.
AUTHORS' CONCLUSIONS
This review found inconclusive evidence to decide on the use of creatine analogues in clinical practice. In particular, it is not clear whether there is an effect on mortality, progression of myocardial infarction and ejection fraction, while there is some evidence that dysrhythmia and dyspnoea might improve. However, it is not clear which analogue, dose, route of administration, and duration of therapy is most effective. Moreover, given the small sample size of the discussed trials and the heterogeneity of the population included in these reports, larger clinical studies are needed to confirm these observations.
Topics: Cardiovascular Diseases; Creatine; Creatine Kinase; Heart Failure; Humans; Hypertension; Molecular Targeted Therapy; Myocardial Infarction; Myocardial Ischemia; Phosphocreatine
PubMed: 22071819
DOI: 10.1002/14651858.CD005184.pub2