Cardiac troponin I in aortic valve disease

Nunes, José Pedro L.; Garcia, J.M. Mota; Farinha, Rui; Silva, João Carlos; Magalhães, Diogo; Pinheiro, Luı́s Vidal; Lima, Cassiano Abreu

doi:10.1016/s0167-5273(02)00502-8

Cited by 34 publications

(27 citation statements)

References 12 publications

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“…It is well recognized that left ventricular hypertrophy can lead to occult subendocardial ischemia via increased oxygen demand from increased muscle mass, coupled with decreased flow reserve due to remodeled coronary microcirculation. Similar observations have been made in the setting of aortic valve disease, in which elevated troponin level was associated with greater left ventricular wall thickness and higher pulmonary artery systolic pressures (22).…”

Section: Nonthrombotic Mechanisms Of Troponin Elevation Demand Ischemiasupporting

confidence: 75%

“…This may be due to excessive wall tension or "myocardial strain," with resulting myofibrillary damage. Myocardial strain may be defined as the percentage change of a structure from its initial length with the application of stress (22). Support for the "strain" theory comes from multiple studies that demonstrate a close correlation between troponin and B-type natriuretic peptide (34), a marker of right and left ventricular wall strain.…”

Section: Myocardial Strainmentioning

confidence: 99%

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Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels when Acute Coronary Syndromes Are Excluded

2005

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Current guidelines for the diagnosis of non-ST-segment elevation myocardial infarction are largely based on an elevated troponin level. While this rapid and sensitive blood test is certainly valuable in the appropriate setting, its widespread use in a variety of clinical scenarios may lead to the detection of troponin elevation in the absence of thrombotic acute coronary syndromes. Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure, can be associated with an increase in troponin level. These elevations may arise from various causes other than thrombotic coronary artery occlusion. Given the lack of any supportive data at present, patients with nonthrombotic troponin elevation should not be treated with antithrombotic and antiplatelet agents. Rather, the underlying cause of the troponin elevation should be targeted. However, troponin elevation in the absence of thrombotic acute coronary syndromes still retains prognostic value. Thus, cardiac troponin elevations are common in numerous disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome. While troponin is a sensitive biomarker to "rule out" non-ST-segment elevation myocardial infarction, it is less useful to "rule in" this event because it may lack specificity for acute coronary syndromes. Ann Intern Med. 2005;142:786-791. www.annals.org For author affiliations, see end of text.

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Section: Nonthrombotic Mechanisms Of Troponin Elevation Demand Ischemiasupporting

confidence: 75%

Section: Myocardial Strainmentioning

confidence: 99%

Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels when Acute Coronary Syndromes Are Excluded

2005

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“…9 The 99th percentile for the distribution of plasma biomarkers was studied at our institution in 305 normal persons. 10 The patients underwent coronary angiography in one of these contexts: AMI with ST-segment elevation or new left bundle branch block, either aiming at primary percutaneous coronary intervention (PCI), or because of persistent or recurrent ischemia, or due to the presence of ischemia in noninvasive testing; AMI without ST segment elevation or new left bundle branch block, because of persistent or recurrent ischemia, or due to the presence of ischemia in noninvasive testing. PCI was performed in 80 patients (63%), and in every case was accompanied by stenting (sirolimus-eluting stents were used in 3 patients).…”

Section: Methodsmentioning

confidence: 99%

Glomerular Filtration Rate and Coronary Artery Disease Burden in Patients with Acute Coronary Syndrome

Nunes

Faria

Garcia

et al. 2007

Clinical Cardiology

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SummaryBackground: Mild renal dysfunction may be associated with increased cardiovascular morbidity and mortality.Methods: The relation between estimated glomerular filtration rate (eGFR), as calculated from plasma creatinine at admission, and coronary artery disease burden (CADB), was studied in a cohort of 110 patients with acute coronary syndrome and coronary atherosclerosis.Results: A relatively weak but significant negative correlation was found between eGFR and CADB as measured by angiography (coefficient correlation of −0.26, probability value of 0.006); a similar association was seen in multiple regression analysis, taking CADB as dependent variable, and eGFR, age, plasma calcium and plasma phosphorus as independent variables. After dividing the 110 patients into eGFR tertiles (with mean values of 102.9 ± 22.8, n = 37, 75.7 + or − 5.6, n = 36, and 53.1 ± 13.4, n = 37, all in mL/min per 1.73 m 2 ), mean CADB values of the lower and higher eGFR tertiles were found to be significantly different (270.6 ± 176.4 and 192.9 ± 78.5, respectively). Similar mean values for CADB and for eGFR were noted when patients with elevated ST segment/new left bundle branch block and patients with nonelevated ST segment acute coronary syndrome were compared.Conclusions: We conclude that renal function of patients with acute coronary syndromes and coronary

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“…Recent data also showed hs-TN elevations in diseases such as renal failure, sepsis, pulmonary embolism, atrial fibrillation (AF), stroke and others [7,8,9,10,11,12,13,14]. Elevation of troponins were associated with stroke severity on hospital admission, insular cortex lesions, short- and long-term clinical outcome and increased risk of mortality, in particular when other risk factors are considered [15,16].…”

Section: Introductionmentioning

confidence: 99%

What Does Elevated High-Sensitive Troponin I in Stroke Patients Mean: Concomitant Acute Myocardial Infarction or a Marker for High-Risk Patients

et al. 2013

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Background: Acute ischemic stroke patients may occasionally suffer from concomitant acute coronary syndrome (ACS). Troponin I and T are established biomarkers to detect ACS. Recently introduced high-sensitive cardiac troponin (hs-TNI and hs-TNT) assays are increasingly used to identify ACS in stroke patients even without signs or symptoms of ACS. These new test systems very often detect elevated values of hs-troponin, although clinical relevance and consequences of elevated hs-TNI values in these patients are unclear so far. Patients and Methods: We examined hs-TNI values in 834 consecutive ischemic stroke patients admitted to our Comprehensive Stroke Center during a 1-year period. hs-TNI was measured immediately after admission and after 3 h if initial hs-TNI was elevated above the 99th percentile of normal values (>0.045 ng/ml). Patients with elevated values were divided into two groups: (1) constant and (2) dynamic hs-TNI values. The dynamic approach was defined as a 30% rise or fall of the hs-TNI value above the critical value within 3 h. All patients received stroke diagnostic and continuous monitoring according to international stroke unit standards, including a 12-lead ECG, blood pressure, body temperature and continuous ECG monitoring, as well as regular 6-hourly neurological and general physical examination (including NIHSS scores). The cardiologists - as members of the Stroke Unit team - evaluated clinical symptoms/examination, as well as laboratory, echocardiographic and ECG findings for the diagnosis of ACS. Results: 172/834 (20.6%) patients showed elevated hs-TNI levels on admission. Patients with elevated hs-TNI values exhibited a significantly (p < 0.001) increased rate of hypertension (89 vs. 77.2%), history of stroke (24.4 vs. 14.8%), history of coronary artery disease (65.7 vs. 34.1%), history of myocardial infarction (22.1 vs. 7.6%), heart failure (12.8 vs. 5.7%) and atrial fibrillation (44.2 vs. 23.6%). 82/136 patients showed constant and 54/136 patients dynamic hs-TNI values: among the latter, 5 patients were diagnosed with ST segment elevation myocardial infarction (STEMI) and 24 with non-STEMI (NSTEMI). Conclusion: Our data demonstrate that hs-TNI was elevated in about 20.6% of acute ischemic stroke patients but therapeutically relevant ACS was diagnosed only in the dynamic group. hs-TNI elevations without dynamic changes may occur in stroke patients without ACS due to different reasons that stress the heart. Therefore, we suppose that hs-TNI is a sensitive marker to detect high-risk patients but serial measurements are mandatory and expert cardiological workup is essential for best medical treatment and to accurately diagnose ACS in acute ischemic stroke patients.

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Cardiac troponin I in aortic valve disease

Cited by 34 publications

References 12 publications

Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels when Acute Coronary Syndromes Are Excluded

Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels when Acute Coronary Syndromes Are Excluded

Glomerular Filtration Rate and Coronary Artery Disease Burden in Patients with Acute Coronary Syndrome

What Does Elevated High-Sensitive Troponin I in Stroke Patients Mean: Concomitant Acute Myocardial Infarction or a Marker for High-Risk Patients

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