Pre-Existing Cardiac Disease, Troponin I Elevation and Mortality in Patients with Severe Sepsis and Septic Shock

Abstract

A prospective, observational study was undertaken to determine the frequency of troponin I elevation and the incidence of pre-existing cardiac disease in patients with severe sepsis and septic shock, and to determine their relationship to mortality. The setting was the surgical intensive care unit of a tertiary care medical centre. Sixty-six consecutive patients admitted with severe sepsis or septic shock requiring pulmonary artery catheterisation for haemodynamic monitoring were studied. Measurement of troponin I was done at the time of pulmonary artery catheterisation and every six to eight hours if there was ongoing tachycardia, hypotension or arrhythmias requiring treatment. Preexisting cardiac disease was determined from the patient and/or family members as well as from the medical record. Significant cardiac history was defined as prior myocardial infarction; abnormal treadmill report, nuclear medicine study or coronary angiogram; history of congestive heart failure or arrhythmia requiring treatment. Forty-two patients (64%) had elevated troponin I at study entrance and 23 patients (35%) had pre-existing cardiac disease. History of cardiac disease was associated with reduced cardiac index and oxygen delivery, and a nearly three-fold increase in mortality (44% vs. 16%, P=0.03), irrespective of elevated troponin I levels. Troponin I elevation alone was not associated with increased mortality. We conclude that pre-existing cardiac disease and elevated troponin I are commonly found in surgical patients with severe sepsis and septic shock. In our study, pre-existing cardiac disease, and not troponin I elevation, was associated with increased mortality.

Cardiac ischemia in patients with septic shock randomized to vasopressin or norepinephrine

“…Although our sample size is modest, it is similar to or larger than that of many previous studies evaluating troponin levels in patients with sepsis [15-17,19,20]; however, we cannot exclude the possibility that our study was underpowered to detect differences in important variables. Given that patients in the vasopressin group were also receiving norepinephrine, this study is not a direct comparison of the administration of vasopressin and norepinephrine.…”

Elevated Cardiac Troponin T Levels in Critically Ill Patients with Sepsis

“…Some authors have found cardiac troponin to be an independent predictor of short-or long-term mortality, 8,[25][26][27][28][29] whereas others have not. 30,40,41 Some investigators included relatively small sample sizes, some included all patients with sepsis, and others evaluated only patients with septic shock or severe sepsis. We included all patients across the spectrum of sepsis, but our database cannot discriminate patients according to the severity of the underlying syndrome.…”

Circulating high sensitivity troponin T in severe sepsis and septic shock: distribution, associated factors, and relation to outcome

“…Several studies have reported an association between troponin levels, measured by conventional assays and short-term outcome in severe sepsis or septic shock [8, 9, 12, 13, 15, 27], whereas others have shown no relationship [10, 16]. Recently, a study of a cohort of 159 patients with bacteraemia reported that cTnI measured with a conventional assay is a univariate, but not an independent predictor of outcome [14].…”

“…The mechanism for troponin elevation in these conditions may not be an acute coronary artery occlusion, but rather low-grade cardiomyocyte injury due to an unfavourable myocardial milieu [1, 2, 37]. Still, earlier studies of patients with sepsis have reported an association between troponin elevation and left ventricular dysfunction, as assessed by echocardiography and pulmonary artery catheterization [8–10, 12]. Potential contributing factors to troponin elevation in this setting are reduced myocardial blood flow secondary to arterial hypotension, microvascular thrombosis with subsequent myocardial injury and augmented myocardial apoptosis secondary to pro-inflammatory cytokines, including tumour necrosis factor-α, interleukin-1β, and interleukin-6 [1, 2].…”