Pulmonary Hypertension After Heart Transplantation in Patients Bridged with the Total Artificial Heart.

Pulmonary hypertension (PH) among heart transplant recipients is associated with an increased risk of mortality. Pulmonary hemodynamics improves after left ventricular assist device (LVAD) implantation; however, the impact of PH before total artificial heart (TAH) implantation on posttransplant hemodynamics and survival is unknown. This is a single center retrospective study aimed to evaluate the impact of TAH implantation on posttransplant hemodynamics and mortality in two groups stratified according to severity of PH: high (≥3 Woods units [WU]) and low (<3 WU) baseline pulmonary vascular resistance (PVR). Hemodynamic data were obtained from right heart catheterization performed at baseline (before TAH) and posttransplant at 1 and 12 months. Patients in the high PVR group (n = 12) experienced improvement in PVR (baseline = 4.31 ± 0.7; 1-month = 1.69 ± 0.7, p < 0.001; 12-month = 48 ± 0.9, p < 0.001) and transpulmonary gradient (baseline = 15.8 ± 3.3; 1-month = 11.57 ± 5.0, p = 0.07; 12-month = 8.50 ± 4.0, p = 0.008) after transplantation, reaching similar values as the low PVR group at 12 months. The filling pressures improved in the high PVR group after heart transplantation (HT), but remained elevated. There was no significant difference in survival between the two groups at 12 months follow-up. Patients with high PVR who are bridged to transplant with TAH had improvement in PVR at 12 months after transplant, and the degree of PVR did not impact posttransplant survival.

The association of myocardial infarction process of care measures and in-hospital mortality: a report from the NCDR®.

BACKGROUND: The Center for Medicare and Medicaid Services (CMS) publicly reports "core process of care measures" along with 30-day mortality rates for patients with acute myocardial infarction; the American College of Cardiology/American Heart Association has a similar but expanded set of performance measures. METHODS: We sought to determine whether hospital-level adherence with these process performance measures was associated with risk-adjusted in-hospital mortality among 96,340 ST-segment elevation myocardial infarction (STEMI) and 145,832 non-STEMI (NSTEMI) patients in the National Cardiovascular Data Registry® ACTION Registry-Get With the Guidelines™ admitted from January 2007 to March 2011 from 372 US sites. Hospitals were grouped based on risk-adjusted in-hospital mortality: low (20%), middle (60%), and high mortality (20%). RESULTS: The mean (SD) mortality from low to high hospital mortality groups for STEMI was 4.9% (0.9%), 5.8% (0.3%), and 7.0% (0.5%); and that for NSTEMI was 3.3% (0.2%), 4.0% (0.2%), and 4.9% (0.3%). Adherence to individual process measures was high, with composite measure adherences exceeding 88%. Composite adherence for both CMS and American College of Cardiology/American Heart Association performance measures was inversely associated with risk-adjusted hospital mortality. However, the association was low for STEMI hospitals and not significant for NSTEMI hospitals. Variation tended to be higher for CMS measures for higher-mortality hospitals. CONCLUSIONS: Although process performance was associated with hospital mortality, the association was low for STEMI and nonsignificant for NSTEMI hospitals, thus supporting the need to measure complementary metrics of acute myocardial infarction quality of care.

Octreotide for left ventricular assist device-related gastrointestinal hemorrhage: can we stop the bleeding?

Left ventricular support devices (LVADs) are associated with a propensity toward gastrointestinal bleeding. A postulated mechanism is related to gastrointestinal arteriovenous malformations secondary to nonpulsatile flow. We describe a case of LVAD-related, gastrointestinal bleeding successfully treated with a combination of subcutaneous and intramuscular depot formulations of octreotide.

Electrocardiographic ST-segment elevation myocardial infarction in critically ill patients: an observational cohort analysis.

OBJECTIVE: To investigate the specificity of the electrocardiographic diagnosis of ST-segment elevation myocardial infarction in the critical care unit setting. DESIGN: Retrospective observational cohort analysis. SETTING: An 880-bed tertiary care teaching hospital with 120 intensive care unit beds. PATIENTS: The population included medical, surgical, trauma, and neurosurgical intensive care unit patients. INTERVENTIONS: Electrocardiograms were systematically collected to include all consecutive recordings over a 15-month period in which the interpretation software indicated ***ACUTE MI***. Patient demographics, markers of intensive care unit complexity, and hospital mortality were ascertained. The electrocardiograms were then further evaluated by a blinded, board-certified cardiologist for agreement or disagreement with the interpretation software. Serum troponin measurements obtained within 96 hrs of electrocardiogram acquisition were used to determine the likelihood of myocardial infarction. MEASUREMENTS AND MAIN RESULTS: Over the 15-month study period, the interpretation software diagnosed ST-segment elevation myocardial infarction in 67 of 2243 intensive care unit patients (2.99%) who had an electrocardiogram performed. In the final study population of 46 cases with electrocardiographic ST-segment elevation myocardial infarction, 85% had peak troponin elevation<5 ng/mL, a strong suggestion against clinical ST-segment elevation myocardial infarction. The cardiologist agreed with the computer interpretation in 39% (18 of 46) of cases, but of those 18 patients, only six showed a significant rise in the troponin level. The cardiologist disagreed with the computer interpretation in 60.9% (28 of 46) of cases and of those, one patient had a marked elevation of the cardiac troponin. CONCLUSIONS: ST-segment elevation myocardial infarction in the intensive care unit is a relatively common electrocardiographic reading both by standard interpretation software and by expert evaluation. In contrast to nonintensive care unit patients who present with chest pain, the electrocardiographic ST-segment elevation myocardial infarction diagnosis seems to be a nonspecific finding in the intensive care unit that is frequently the result of a variety of nonischemic processes. The vast majority of such patients do not have frank ST-segment elevation myocardial infarction.

Recurrent, severe, and rapidly reversible apical ballooning syndrome in status asthmaticus.

Apical ballooning syndrome, or Tako-tsubo cardiomyopathy, is a peculiar form of transient left-ventricular dysfunction originally described as triggered by emotional stress. Subsequent reports indicated that physical stressors can also induce this clinical syndrome. We describe for the first time, to the best of our knowledge, a case of recurrent, severe, and quickly reversible apical ballooning syndrome provoked by the use of high-dose inhaled ß-adrenergic agonists in status asthmaticus.

Brugada-pattern electrocardiogram in propranolol intoxication.

Brugada syndrome is characterized by the electrocardiographic (ECG) pattern of right bundle-branch block (RBBB) with a high take-off, coved ST-segment elevation in the precordial leads V1 to V3, and the risk of sudden cardiac death. Typically, there is no evidence of structural heart disease. In many cases, Brugada syndrome has been linked to a mutation of the gene SCN5A, which encodes for the fast cardiac sodium channel. In patients with the Brugada syndrome, pharmacologic sodium channel blockade can increase the degree of ST-segment elevation. Interestingly, even in patients with a normal baseline ECG and no clinical suggestion of the Brugada syndrome, toxic doses of class I antiarrhythmic agents as well as toxicities with several nonantiarrhythmic drugs that possess sodium channel blocking properties can induce the Brugada ECG abnormality. Specifically, the beta-receptor blocker propranolol, at high doses, binds to the cardiac sodium channels and inhibits sodium uptake. In this report, we describe a case of severe propranolol toxicity, which resulted in the Brugada ECG pattern in an otherwise healthy individual who had no clinical or ECG suggestion of the genetically determined Brugada syndrome.

Significance of respiratory artifact in the electrocardiogram.

Electrocardiographic artifact is generally considered to be a nuisance. Respiratory artifact, however, is a physiologic signal that may carry useful diagnostic information. Our goal was to evaluate the characteristics, prevalence, and clinical significance of respiratory artifact observed in electrocardiograms (ECGs). ECGs exhibiting repetitive microoscillations were systematically collected. The morphologic characteristics of the microoscillations were analyzed and their association with the respiratory cycle was evaluated using simultaneous respiratory waveform tracings. The presence and rate of respiratory artifact were correlated with the patient's clinical status, including medical diagnoses and the need for ventilatory support. During a 30-month period, respiratory artifact was detected in 320 12-lead ECGs. It was best seen in leads II, III, aVF, and V5. Respiratory artifact occurred during the inspiratory phase and its rate correlated precisely with objective measures of the respiratory rate. The majority of patients with respiratory artifact revealed diseases of the respiratory (26.6%) and circulatory systems (24.0%) and, of note, respiratory artifact was never detected in patients with normal cardiorespiratory function; 43.5% of patients with respiratory artifact required ventilatory support, including 28.2% requiring continuous mechanical ventilation. Successful treatment of the underlying condition resulted in a decrease in the rate or in complete disappearance of the respiratory artifact. In conclusion, respiratory artifact is commonly seen in routine 12-lead ECGs of hospitalized patients. It is associated with a high-risk state of increased work of breathing due to either compromised cardiac or pulmonary function. Additionally, the presence of respiratory artifact enables precise evaluation of the respiratory rate-a commonly miscalculated vital sign.