Hyponatremia and long-term mortality in survivors of acute ST-elevation myocardial infarction.

BACKGROUND: Hyponatremia, a marker of neurohormonal activation, is a common electrolyte disorder among patients with acute ST-elevation myocardial infarction. The long-term prognostic value of hyponatremia during the acute phase of infarction is not known. METHODS: We studied 978 patients with acute ST-elevation myocardial infarction and without a history of heart failure who survived the index event. During the hospital stay, sodium levels were obtained on admission and at 24, 48, and 72 hours. The median duration of follow-up after hospital discharge was 31 months (range, 9-61 months). RESULTS: Hyponatremia, defined as a mean serum sodium level less than 136 mEq/L, was present during admission in 108 patients (11.0%). In a multivariable Cox proportional hazards model adjusting for other potential clinical predictors of mortality and for left ventricular ejection fraction, hyponatremia during admission remained an independent predictor of postdischarge death (hazard ratio [HR], 2.0; 95% confidence interval [CI], 1.3-3.2; P = .002). Hyponatremia during admission was also independently associated with postdischarge readmission for heart failure (HR, 1.6; 95% CI, 1.1-2.6; P = .04). When serum sodium level was used as a continuous variable, the adjusted HR for death or heart failure was 1.12 for every 1-mEq/L decrease (95% CI, 1.07-1.18; P<.001). CONCLUSION: Hyponatremia in the early phase of ST-elevation myocardial infarction is a predictor of long-term mortality and admission for heart failure after hospital discharge, independent of other clinical predictors of adverse outcome and left ventricular ejection fraction.

Inhospital and 1-year mortality of patients who develop worsening renal function following acute ST-elevation myocardial infarction.

BACKGROUND: Recent studies have emphasized the prognostic value of baseline creatinine or estimated creatinine clearance in the setting of acute coronary syndromes. However, the prevalence and prognostic significance of worsening renal function (WRF) in patients with acute ST-elevation myocardial infarction are unknown. METHODS: We studied 1038 patients presenting with acute ST-elevation infarction. WRF was defined as an increase of > or =0.5 mg/dL in creatinine level at any point during hospital stay. The relation between WRF and subsequent inhospital and 1-year mortality was analyzed by use of multivariate logistic regression and Cox proportional hazards models, respectively, controlling for covariates. RESULTS: WRF occurred in 98 (9.6%) patients during hospital stay. Baseline renal dysfunction (calculated glomerular filtration rate <60 mL/min) and WRF were strong independent predictors of inhospital mortality (adjusted odds ratios 2.8, 95% CI 1.3-5.9; and 11.4, 95% CI 6.6-19.5, respectively). In a Cox multivariate analysis, both baseline renal dysfunction (adjusted hazard ratio 2.8, 95% CI 1.6-4.9) and WRF (adjusted hazard ratio 7.2, 95% CI 4.9-10.4) remained independent predictors of 1-year mortality. WRF provided incremental prognostic value toward the prediction of 1-year mortality when added to clinical risk predictors and baseline renal function. The increased mortality associated with impaired baseline renal function was largely caused by events occurring in patients with WRF. CONCLUSION: WRF occurring during admission for ST-elevation myocardial infarction is a powerful and independent predictor of inhospital and 1-year mortality. Small elevations of serum creatinine may serve as a simple marker to identify patients at a very high risk.

Prognostic importance of hyponatremia in acute ST-elevation myocardial infarction.

PURPOSE: To determine the prevalence and prognostic implications of hyponatremia in the setting of acute ST-elevation myocardial infarction. METHODS: The study sample consisted of 1047 consecutive patients presenting with acute ST-elevation myocardial infarction. Plasma sodium concentrations were obtained on admission and at 24, 48, and 72 hours thereafter. Infarct size was determined by echocardiographic examination that was performed on day 2 or 3 of hospitalization. RESULTS: Hyponatremia, defined as a plasma sodium level <135 mmol/L (<135 mEq/L), was present on admission in 131 patients (12.5%) and developed during the first 72 hours of hospitalization in 208 patients (19.9%). Plasma sodium levels decreased to < or = 130 mmol/L in 45 patients (4.3%). In a multivariate logistic regression analysis, hyponatremia was independently associated with 30-day mortality. The risk of 30-day mortality associated with hyponatremia on admission (odds ratio [OR] = 2.0; 95% confidence interval [CI]: 1.0 to 3.9; P = 0.04) was similar to that of hyponatremia developing after admission (OR = 2.4; 95% CI: 1.5 to 4.2; P = 0.002). The risk of 30-day mortality increased with the severity of hyponatremia, with an odds ratio of 2.1 in patients with sodium levels between 130 and 134 mmol/L (95% CI: 1.2 to 3.5; P = 0.007) and 3.4 in those with levels <130 mmol/L (95% CI: 1.5 to 7.8; P = 0.002). CONCLUSION: Hyponatremia on admission or early development of hyponatremia in patients with acute ST-elevation myocardial infarction is an independent predictor of 30-day mortality, and prognosis worsens with the severity of hyponatremia. Further studies are required to determine if plasma sodium levels may serve as a simple marker to identify patients at high risk.

Staged versus one-step approach for multivessel percutaneous coronary interventions.

BACKGROUND: Percutaneous coronary interventions (PCIs) in patients with multivessel coronary artery disease (CAD) may be staged or performed in a single session. No data exist about the relative safety and efficacy of these 2 strategies. Our aim was to compare short-term and long-term outcomes of patients with multivessel CAD who underwent PCI in 1 versus 2 sessions. METHODS AND RESULTS: The study included 264 consecutive patients who underwent treatment in our center during 1997 and 1998. PCI was conducted in a single session in 129 patients and was staged in 135 patients. The mean interval between the sessions in the staged group was 45.6 +/- 22.3 days. The rates of major adverse cardiac events (MACEs) during in-hospital stay did not differ significantly between the staged (combined for both stages) and nonstaged groups (2.2% vs 4.6%; P =.28). A trend for lower event rates at 30-day (2.9% vs 6.9%; P =.13) and 1-year follow-up (26.1 vs 35.9; P =.08) favored the staged arm. Diameter stenosis > or =50% was found in 17% of patients in the staged group in the second session and was successfully retreated in most of them. No MACE occurred between the sessions. Multivariate analysis identified staging of the procedure as a single independent predictor of MACE at 1-year follow-up (P =.05). CONCLUSION: Our results suggest that a practical staging strategy within 4 to 8 weeks is safe and allows for identification and treatment of potential excessive proliferative response in the previously intervened lesions during the second procedure.

Diagnostic coronary angiography induces a systemic inflammatory response in patients with stable angina.

BACKGROUND: Systemic markers of inflammation increase after percutaneous coronary intervention (PCI). The rise in inflammatory markers after PCI is frequently attributed to the inflammatory stimulus associated with coronary artery injury during balloon inflation and coronary stent implantation. The aim of this study was the determine whether diagnostic coronary angiography performed in patients with stable angina triggers a systemic inflammatory response. METHODS: We prospectively studied patients with chronic stable angina undergoing either coronary angiography (n = 13) or coronary angiography followed by PCI (n = 13). Peripheral blood samples were obtained before and 24 hours, 48 hours, and 4 weeks after the procedure and analyzed for C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Patients with periprocedural myocardial necrosis were excluded. RESULTS: There was a significant increase in CRP levels at 24 and 48 hours in both the coronary angiography (P <.05) and PCI (P <.01) groups. IL-6 levels peaked at 24 hours in both the coronary angiography (median, 2.5-9.5 pg/mL; P =.01) and PCI (median, 3.0-8.2 pg/mL; P <.005) groups. At 4 weeks, both CRP and IL-6 returned to baseline levels. TNF-alpha levels were unchanged with either coronary angiography or PCI. The magnitude of the rise of CRP and IL-6 levels was not significantly different between the groups. There was a fair correlation between baseline and peak postprocedural levels of CRP (r = 0.67, P =.008) and IL-6 (r = 0.48, P =.016). CONCLUSION: Uncomplicated diagnostic coronary angiography triggers a systemic inflammatory response in patients with stable angina. The contribution of coronary angiography should be considered in interpreting the significance of the systemic inflammatory response observed after PCI.