Victor G. Dávila-Román

Cardiac troponin I. A marker with high specificity for cardiac injury.

BackgroundLevels of MBCK can be increased in patients with skeletal muscle injury or renal failure in the absence of myocardial injury, causing diagnostic confusion. This study was designed to determine whether measurement of cardiac troponin I (cTnI), a myocardial regulatory protein with comparable sensitivity to MBCK, has sufficient specificity to clarify the etiology of MBCK elevations in patients with acute or chronic skeletal muscle disease or renal failure. Methods and ResultsOf the patients (n=215) studied, 37 had acute skeletal muscle injury, 10 had chronic muscle disease, nine were marathon runners, and 159 were chronic dialysis patients. Patients were evaluated clinically, by ECG, and by two-dimensional echocardiography. Total creatine kinase (normal, <170 IU/L) was determined spectrophotometrically, and cTnI (normal, <3.1 ng/mL) and MBCK (normal, <6.7 ng/mL) were determined with specific monoclonal antibodies. Values above the upper reference limit were considered “elevated.” Elevations of total creatine kinase were common, and elevations of MBCK occurred in 59%o of patients with acute muscle injury, 78% of patients with chronic muscle disease and marathon runners, and 3.8% of patients with chronic renal failure. Some of the patients were critically ill; five patients were found to have had myocardial infarctions and one had a myocardial contusion. cTnI was elevated only in these patients. ConclusionElevations of cTnI are highly specific for myocardial injury. Use of cTnI should facilitate distinguishing whether elevations of MBCK are due to myocardial or skeletal muscle injury.

2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

Jeffrey L. Anderson, MD, FACC, FAHA, Chair Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect Nancy M. Albert, PhD, RN, FAHA Biykem Bozkurt, MD, PhD, FACC, FAHA Ralph G. Brindis, MD, MPH, MACC Lesley H. Curtis, PhD, FAHA David DeMets, PhD[¶¶][1] Lee A. Fleisher, MD, FACC, FAHA Samuel

Diagnosis of Perioperative Myocardial Infarction with Measurement of Cardiac Troponin I

BACKGROUND Perioperative myocardial infarction is the most common cause of morbidity and mortality in patients who have had noncardiac surgery, but its diagnosis can be difficult. The present study was designed to determine whether the measurement of serum levels of cardiac troponin I, a highly sensitive and specific marker for cardiac injury, would help establish the diagnosis of myocardial infarction. METHODS We obtained preoperative measurements of MB creatine kinase, total creatine kinase, and cardiac troponin I, in addition to base-line electrocardiograms and two-dimensional echocardiograms, in 96 patients undergoing vascular surgery and 12 undergoing spinal surgery. Blood samples were obtained every 6 hours for at least the first 36 hours after surgery, and electrocardiograms were obtained daily; a second echocardiogram was obtained approximately three days after surgery. The appearance of a new abnormality in segmental-wall motion on the postoperative echocardiogram (that is, an abnormality that had not been seen on the preoperative echocardiogram) was considered to be indicative of perioperative infarction. RESULTS Eight patients who underwent vascular surgery had new abnormalities in segmental-wall motion and received a diagnosis of perioperative infarction. All eight had elevations of cardiac troponin I, and six had elevations of MB creatine kinase. Of the 100 patients without perioperative infarction detected by echocardiography, 19 had elevations of MB creatine kinase, and 1 had a slight elevation of cardiac troponin I. CONCLUSIONS The measurement of cardiac troponin I is a sensitive and specific method for the diagnosis of perioperative myocardial infarction. It avoids the high incidence of false diagnoses associated with the use of MB creatine kinase as a diagnostic marker.

Risk Factors for Early or Delayed Stroke After Cardiac Surgery

BACKGROUND Stroke after cardiac surgery is a devastating complication that leads to excess mortality and health resource utilization. The purpose of this study was to identify risk factors for perioperative stroke, including strokes detected early after cardiac surgery or postoperatively. METHODS AND RESULTS Data were obtained from 2972 patients undergoing coronary artery bypass graft and/or valve surgery. Patients >/=65 years old and those with a history of symptomatic neurological disease underwent preoperative carotid artery ultrasound scanning. Intraoperative epiaortic ultrasound to assess for ascending aorta atherosclerosis was performed in all patients. New strokes were considered as a single end point and were categorized with respect to whether they were detected immediately after surgery (early stroke) or after an initial, uneventful neurological recovery from surgery (delayed stroke). Strokes occurred in 48 patients (1.6%); 31 (65%) were delayed strokes. By multivariate analysis, prior neurological event, aortic atherosclerosis, and duration of cardiopulmonary bypass were independently associated with early stroke, whereas predictors of delayed stroke were prior neurological event, diabetes, aortic atherosclerosis, and the combined end points of low cardiac output and atrial fibrillation. Female sex was associated with a 6.9-fold increased risk of early stroke and a 1.7-fold increased risk of delayed stroke. In-hospital mortality of patients with early (41%) and delayed (13%) strokes was higher than that of other patients (3%, P=0.0001). CONCLUSIONS Most strokes after cardiac surgery occurred after initial uneventful recovery from surgery. Women were at higher risk to suffer early and delayed perioperative strokes. Atrial fibrillation had no impact on postoperative stroke rate unless it was accompanied by low cardiac output syndrome.

Altered myocardial fatty acid and glucose metabolism in idiopathic dilated cardiomyopathy

OBJECTIVES The purpose of this study was to determine whether patients with idiopathic dilated cardiomyopathy (IDCM) exhibit alterations in myocardial fatty acid and glucose metabolism. BACKGROUND Alterations in myocardial metabolism have been implicated in the pathogenesis of heart failure (HF); however, studies of myocardial metabolic function in human HF have yielded conflicting results. Animal models of HF have shown a downregulation of the expression of enzymes of fatty acid beta-oxidation that recapitulates the fetal energy metabolic program, in which fatty acid metabolism is decreased and glucose metabolism is increased. METHODS Seven patients with IDCM (mean left ventricular ejection fraction 27 +/- 8%) and 12 normal controls underwent positron emission tomography for measurements of myocardial blood flow (MBF), myocardial oxygen consumption (MVO(2)), myocardial glucose utilization (MGU), myocardial fatty acid utilization (MFAU) and myocardial fatty acid oxidation (MFAO). RESULTS The systolic and diastolic blood pressures, plasma substrates and insulin levels, MBF and MVO(2), were similar between groups. The rates of MFAU and MFAO were significantly lower in IDCM than in the normal control group (MFAU: 134 +/- 44 vs. 213 +/- 49 nmol/g/min, p = 0.003; and MFAO: 113 +/- 50 vs. 205 +/- 49 nmol/g/min, p = 0.001) and the rates of MGU were significantly higher in IDCM than the normal control group (MGU: 247 +/- 63 vs. 125 +/- 64 nmol/g/min, p < 0.001). CONCLUSIONS Patients with IDCM exhibit alterations in myocardial metabolism characterized by decreased fatty acid metabolism and increased myocardial glucose metabolism, a pattern similar to that shown in animal models of HF. Whether alterations in myocardial metabolism constitute an adaptive response or mediate the development of HF remains to be determined.

Prevalence of Depression in Hospitalized Patients With Congestive Heart Failure

Objective Prevalence estimates of depression in hospitalized patients with congestive heart failure (CHF) differ considerably across studies. This article reports the prevalence of depression in a larger sample of hospitalized patients with CHF and identifies demographic, medical, psychosocial, and methodological factors that may affect prevalence estimates. Methods A modified version of the Diagnostic Interview Schedule was administered to a series of 682 hospitalized patients with CHF to determine the prevalence of DSM-IV major and minor depression; 613 patients also completed the Beck Depression Inventory. Medical, demographic, and social data were obtained from hospital chart review, echocardiography, and patient interview. Results In the sample as a whole, 20% of the patients met the DSM-IV criteria for a current major depressive episode, 16% for a minor depressive episode, and 51% scored above the cutoff for depression on the Beck Depression Inventory (≥10). However, the prevalence of major depression differed significantly between strata defined by the functional severity of heart failure, age, gender, employment status, dependence in activities of daily living, and past history of major depression. For example, the prevalence ranged from as low as 8% among patients in New York Heart Association class I failure to as high as 40% among patients in class IV. Conclusions The prevalence of depression in hospitalized patients with CHF is similar to rates found in post-myocardial infarction patients. However, it is considerably higher in certain subgroups, such as patients with class III or IV heart failure. Further research is needed on the prognostic importance and treatment of comorbid depression in CHF.

Replacement of the aortic root with a pulmonary autograft in children and young adults with aortic-valve disease

BACKGROUND The optimal substitute for severely diseased aortic valves in children and young adults is unknown. The use of a mechanical prosthesis requires permanent treatment of the patient with anticoagulants and is associated with thromboembolic and hemorrhagic complications. Aortic-valve allografts and porcine bioprostheses, which do not necessitate anticoagulant therapy, may deteriorate and have limited durability. METHODS We therefore evaluated the use of the autologous pulmonary valve (i.e., the patients own pulmonary valve) and the adjacent pulmonary artery as a replacement for the aortic valve and aortic sinuses in 33 patients. Five of the patients were from 8 to 16 years of age, and 28 were from 20 to 47 years of age. The pulmonary valve and the main pulmonary artery were used to replace the diseased aortic valve and the adjacent aorta. The coronary arteries were detached from the aorta and implanted into the pulmonary artery. The pulmonary valve and artery were replaced with a cryopreserved pulmonary allograft. RESULTS There were no deaths during follow-up of up to 48 months (mean, 21 months). There were no episodes of infective endocarditis, and no reoperations on the aortic root were necessary. Also, there was no evidence on echocardiography of progressive dilatation of the autografts. With color-flow Doppler imaging, 22 patients were found to have only trivial regurgitation or none, 9 patients to have mild regurgitation, and no patients to have moderate or severe regurgitation across the autograft at the most recent follow-up visit. The mean peak velocity of flow across the autograft was 1.3 m per second (upper limit of normal, 1.8), indicating the absence of stenosis. One patient required reoperation for stenosis of the pulmonary allograft. CONCLUSIONS Although the pulmonary-autograft procedure is more complex than simple aortic-valve replacement, it has been safely applied in selected patients, including young adults. Intermediate follow-up indicates satisfactory function of the autografts, with no dilatation or progressive valvular regurgitation. Pulmonary-root autografts may thus be the best available substitute for diseased aortic valves in children and young adults.

Low-Dose Dopamine or Low-Dose Nesiritide in Acute Heart Failure With Renal Dysfunction The ROSE Acute Heart Failure Randomized Trial

IMPORTANCE Small studies suggest that low-dose dopamine or low-dose nesiritide may enhance decongestion and preserve renal function in patients with acute heart failure and renal dysfunction; however, neither strategy has been rigorously tested. OBJECTIVE To test the 2 independent hypotheses that, compared with placebo, addition of low-dose dopamine (2 μg/kg/min) or low-dose nesiritide (0.005 μg/kg/min without bolus) to diuretic therapy will enhance decongestion and preserve renal function in patients with acute heart failure and renal dysfunction. DESIGN, SETTING, AND PARTICIPANTS Multicenter, double-blind, placebo-controlled clinical trial (Renal Optimization Strategies Evaluation [ROSE]) of 360 hospitalized patients with acute heart failure and renal dysfunction (estimated glomerular filtration rate of 15-60 mL/min/1.73 m2), randomized within 24 hours of admission. Enrollment occurred from September 2010 to March 2013 across 26 sites in North America. INTERVENTIONS Participants were randomized in an open, 1:1 allocation ratio to the dopamine or nesiritide strategy. Within each strategy, participants were randomized in a double-blind, 2:1 ratio to active treatment or placebo. The dopamine (n = 122) and nesiritide (n = 119) groups were independently compared with the pooled placebo group (n = 119). MAIN OUTCOMES AND MEASURES Coprimary end points included 72-hour cumulative urine volume (decongestion end point) and the change in serum cystatin C from enrollment to 72 hours (renal function end point). RESULTS Compared with placebo, low-dose dopamine had no significant effect on 72-hour cumulative urine volume (dopamine, 8524 mL; 95% CI, 7917-9131 vs placebo, 8296 mL; 95% CI, 7762-8830 ; difference, 229 mL; 95% CI, -714 to 1171 mL; P = .59) or on the change in cystatin C level (dopamine, 0.12 mg/L; 95% CI, 0.06-0.18 vs placebo, 0.11 mg/L; 95% CI, 0.06-0.16; difference, 0.01; 95% CI, -0.08 to 0.10; P = .72). Similarly, low-dose nesiritide had no significant effect on 72-hour cumulative urine volume (nesiritide, 8574 mL; 95% CI, 8014-9134 vs placebo, 8296 mL; 95% CI, 7762-8830; difference, 279 mL; 95% CI, -618 to 1176 mL; P = .49) or on the change in cystatin C level (nesiritide, 0.07 mg/L; 95% CI, 0.01-0.13 vs placebo, 0.11 mg/L; 95% CI, 0.06-0.16; difference, -0.04; 95% CI, -0.13 to 0.05; P = .36). Compared with placebo, there was no effect of low-dose dopamine or nesiritide on secondary end points reflective of decongestion, renal function, or clinical outcomes. CONCLUSION AND RELEVANCE In participants with acute heart failure and renal dysfunction, neither low-dose dopamine nor low-dose nesiritide enhanced decongestion or improved renal function when added to diuretic therapy. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01132846.

Strategy for the reduction of stroke incidence in cardiac surgical patients

Atherosclerosis of the ascending aorta (AAA) and severe carotid artery disease are risk factors for stroke in cardiac surgical patients. Twelve hundred of a consecutive series of 1,334 patients 50 years of age or older having a cardiac operation were screened for the presence of AAA by intraoperative ultrasonographic scanning and for the presence of carotid artery occlusive disease (791 of 798 patients > or = 65 years of age and younger symptomatic patients) by carotid duplex scanning. Coronary artery disease was present in 88% of the patients. Patients with moderate or severe AAA (n = 231; 19.3% of the total) were treated by ascending aortic replacement (n = 27) or by modified, less extensive techniques (n = 168) to avoid the atherosclerotic areas. Thirty-three patients had combined carotid endarterectomy and cardiac operation. Thirty-day mortality and stroke rates for the 1,200 patients were 4.0% and 1.6%, respectively. The stroke rate was low (1.1%) among the 969 patients with no or mild AAA. It was zero among 27 patients with moderate or severe AAA who had ascending aortic replacement and among the 33 patients who had carotid endarterectomy. The stroke rates were higher for 111 patients with moderate or severe ascending aortic disease who had only minor interventions (6.3%) and for 16 patients with severe carotid artery disease who did not have carotid endarterectomy (18.7%). Screening for AAA and carotid artery disease and aggressive surgical treatment of moderate or severe AAA and severe or symptomatic carotid artery disease appears to reduce the frequency of stroke in older cardiac surgical patients.

Atherosclerosis of the ascending aorta. Prevalence and role as an independent predictor of cerebrovascular events in cardiac patients.

The cause of cerebral and peripheral embolism remains undetermined in a significant number of patients. An atherosclerotic thoracic aorta has thus far been considered to be an uncommon one. Methods To define the potential role of the ascending thoracic aorta as an embolic source, intraoperative ultrasonic aortic imaging was performed in 1200 of 1334 consecutive patients aged 50 years and older who were undergoing cardiac surgery. Patients were divided into two groups according to the results of the ultrasound study in terms of presence or absence of atherosclerotic disease. The prevalence of previous neurological events in the two groups was characterized and compared. Results Ascending aortic atherosclerosis was present in 231 (19.3%) of the patients studied. Patients in this category were older (P<.0001). A higher percentage of them were smokers (P<.0001) compared with patients with less severe disease. Coronary artery disease was more extensive (P=.012), and a higher percentage of these patients had a history of peripheral vascular disease (P<.0001). Univariate analysis of the subjects with (n=158) and without (n=1042) previous neurological events indicated that age, body mass index, atrial fibrillation, hypertension, and atherosclerosis of the ascending aorta were associated significantly with previous occurrence of a cerebrovascular accident. For the group as a whole, multiple logistic regression analysis demonstrated that hypertension (odds ratio, 1.81; P=.002), atherosclerosis of the ascending aorta (odds ratio, 1.65; P=.013), and atrial fibrillation (odds ratio, 1.54; P=.060) were significantly and independently associated with the occurrence of previous neurological events. Conclusions Atherosclerosis of the ascending aorta is an independent risk factor for cerebrovascular events. An atherosclerotic ascending aorta may represent a potential source of emboli or may be a marker of generalized atherosclerosis.