Cardiology department versus intensive care unit admission after successful uncomplicated transcatheter aortic valve replacement (TAVR).

BACKGROUND: Most patients after transcatheter aortic valve replacement (TAVR) are admitted directly to the cardiac intensive care unit (CICU) despite low complication rates. Reducing unnecessary CICU hospitalization reduces healthcare costs. This study aimed to compare the outcomes between patients admitted directly to the cardiology department (CD) and those admitted to CICU based on prespecified protocols. METHODS: Historical cohort study of all patients who underwent TAVR and were admitted directly to the CD according to a prespecified protocol (uncomplicated procedure, hemodynamically stable, without new conduction abnormalities) in 2017-2018, and the same number of patients meeting the same criteria who were admitted to the CICU in 2015-2016 before direct CD admission was initiated. Pacemaker implantation during the procedure was not considered a new conduction abnormality. In-hospital outcomes and 30-day post-discharge outcomes were compared. RESULTS: Overall, 260 patients (130 CICU + 130 CD) were included in the study. There was no in-hospital mortality in either group, and the post-procedure length of stay was shorter for patients admitted to CD (median and IQR: 2, 2-4 vs. 4, 3-5 days, p <0.001). There was no significant difference in 30-day emergency department visits between groups (CICU:13.9% vs. CD:16.2%, p = 0.602), rehospitalization rate (9.3%) was the same in both groups, and one patient from the CICU group died. Similar results were observed in multivariable analysis and after matching. CONCLUSION: Direct admission to the CD after TAVR, according to the proposed criteria, may be considered as a safe and less expensive alternative for stable patients after an uncomplicated TAVR procedure.

A patient with pulmonary embolism takes a surprising HIT: a case report.

BACKGROUND: Venous thromboembolism (VTE) is a common condition that may manifest as intermediate or high-risk pulmonary embolism (PE), requiring either primary or subsequent fibrinolytic therapy. In these cases, catheter-directed thrombolysis (CDT) has been shown to be beneficial. CASE SUMMARY: We present the case of a borderline obese but otherwise healthy 43-year-old male individual, who was admitted with acute intermediate- to high-risk PE requiring treatment with intravenous unfractionated heparin. After initial therapy failure, the patient received CDT, with subsequent clinical worsening, and a mixed result of imaging studies suggesting partial central worsening and partial peripheral improvement of the thrombotic burden and right ventricular (RV) function. After a multidisciplinary PE response team (PERT) consultation, the diagnosis of heparin-induced thrombocytopenia (HIT) with normal platelet levels was made. Therapy was changed to intravenous bivalirudin, with an excellent clinical response and complete recovery of RV function. The patient was discharged with oral rivaroxaban therapy, and on follow-up was otherwise well. DISCUSSION: Apparent failure of thrombolytic therapy for VTE warrants a clinical investigation into possible causes of a pro-thrombotic state. In this case, the diagnosis of HIT was surprising, especially due to only a mild decline in platelet levels that were well within normal range. We also acknowledge the significance of our PERT in the key diagnosis made in this case.

Temporal trends in the outcomes of patients with acute myocardial infarction associated with renal dysfunction over the past decade.

BACKGROUND: Patients with renal dysfunction (RD) who present with acute myocardial infarction (AMI) are at a high risk for subsequent cardiovascular morbidity and mortality. We sought to evaluate changes in the short and long term mortality of AMI patients with RD compared to patients with normal renal function over the last decade. METHODS: This study based on 4 bi-annually surveys was performed from 2002 to 2010 and included 9468 AMI patients, that were followed for 1year, of whom 2770 (29%) had reduced estimated GFR ([eGFR]<60ml/min/m(2)). Among patients with reduced eGFR: 1251 patients (45%) were included in the 2002-2005 surveys (early period) and 1519 (55%) in the 2006-2010 surveys (late period). RESULTS: Patients with RD were more likely to have advanced cardiovascular disease, multiple comorbidities and higher in-hospital, 30-day, and 1-year mortality rates (8.1%,12.3% and 23% vs. 0.7%, 1.7% and 4%, respectively; all p<0.001). Patients with RD enrolled during the late survey periods were more likely to undergo primary PCI and be discharged with current evidence based medical treatment. 1-year mortality rates were significantly lower among patients with RD who were enrolled during the late vs. early survey periods: 22% vs. 25% respectively; (Log-rank P-value <0.001). Consistently, multivariate analysis showed that patients with RD who were enrolled during the late survey periods displayed a lower adjusted risk for 1-year mortality (HR 0.83; CI[0.70-0.94] P=0.01). CONCLUSIONS: Prognosis of patients with RD admitted with AMI has significantly improved over the last decade, possibly due to an improvement of pharmacological and non-pharmacological management.

Acute coronary syndromes are associated with a reduction of VLA-1+ peripheral blood T cells and their enrichment in coronary artery plaque aspirates.

Memory T cells producing interferon (IFN)γ and expressing very late antigen-1 (VLA-1) integrin collagen receptors are found in carotid atherosclerotic plaques, suggesting their involvement in coronary artery disease (CAD) as well. To determine the role of VLA-1+ T cells in CAD percent of CD3+ T cells binding monoclonal antibodies (mAb) to VLA-1 in peripheral blood (PB), and in coronary plaque material aspirated during coronary arterography and arterial blood, were analyzed in a cohort of 117 patients with CAD and 34 controls without CAD. % VLA-1+ T cells in PB was 0.63 ± 0.09% in controls compared to 0.96 ± 0.95% in patients with CAD (p<0.009). The increase was due to a marked elevation of % VLA-1+ T cells in stable CAD (1.6 ± 0.27%) whereas % VLA-1+ T cells during acute coronary syndromes (ACS) and in patients with ischemia by thalium SPECT scan had significantly lower levels. % VLA-1+ T cells in coronary artery plaque material aspirated during therapeutic angiography in patients with ACS was significantly higher than in arterial blood (1.39 ± 0.96% vs 0.75 ± 0.84%, p<0.035, n=3). Thus, % VLA-1+ T cells increases in the PB during stable CAD but decreases in ACS. The finding of their enrichment in coronary blood containing atherosclerotic plaque aspirates suggests that a shift of VLA-1+ T cells from blood to atherosclerotic plaques may play a role in plaque instability in patients with ACS.

Safety of intra-aortic balloon pump using glycoprotein IIb/IIIa antagonists.

BACKGROUND: Anticoagulation with heparin is recommended with intra-aortic balloon pump (IABP) to prevent thrombosis and embolization. However, anticoagulation increases the risk of bleeding, particularly in combination with glycoprotein (GP) IIb/IIIa antagonists. HYPOTHESIS: We investigated the safety of using GP IIb/IIIa antagonists without heparin after IABP insertion in patients who underwent primary percutaneous coronary intervention (PCI). METHODS: Consecutive patients with acute myocardial infarction (AMI), who underwent primary PCI and were treated with GP IIb/IIIa antagonists without concomitant heparin, and in whom IABP was inserted, were followed during hospitalization for thrombotic and hemorrhagic complications. RESULTS: Ninety-seven patients were included in this analysis. Glycoprotein IIb/IIIa antagonist treatment duration was 12-24 h in 89% of patients, and IABP duration was up to 48 h in 97% of patients. Three patients (3.1%) developed vascular complications: 1 had a major limb ischemia (long IABP treatment), 1 had a minor limb ischemia, and 1 had a cerebrovascular event (after prolonged resuscitation). All patients were already on heparin at the time of the thrombotic events. The rates of major and minor bleeding complications were 9% and 15.5%, respectively. CONCLUSIONS: The rate of thrombotic complications is relatively low in post-primary PCI patients with IABP treated with GP IIb/IIIa antagonists without concomitant heparin therapy. Such an approach may reduce the risk of hemorrhagic complications, with low risk of thrombotic complications.

Long-term prognostic significance of left atrial volume in acute myocardial infarction.

OBJECTIVES: The aim of this study was to evaluate the significance of increased left atrial (LA) volume determined within the first 48 h of admission as a long-term predictor of outcome in patients with acute myocardial infarction (MI). BACKGROUND: The LA volume reflects left ventricular (LV) diastolic properties. Whereas other LV Doppler diastolic characteristics are influenced by acute changes in LV function, LA volume is stable and reflects diastolic properties before MI. METHODS: Clinical and echocardiographic parameters were prospectively collected in 395 consecutive patients with acute MI. Patients with LA volume index (LAVI) >32 ml/m(2) (normal + 2 standard deviations) were compared with those with LAVI <==32 ml/m(2). Independent clinical and echocardiographic prognostic risk factors for five years' mortality were determined by the Cox proportional hazard model. RESULTS: Left atrial volume index >32 ml/m(2) was found in 63 patients (19%) who had a higher incidence of congestive heart failure on admission (24% vs. 12%, p < 0.01), a higher incidence of mitral regurgitation, increased LV dimensions, and reduced LV ejection fraction when compared with patients with LAVI <==32 ml/m(2). Their five-year mortality rate was 34.5% versus 14.2% (p < 0.001). Significant independent risk predictors of five years' mortality were age (10 years) (odds ratio [OR] 1.45; 95% confidence interval [CI]1.14 to 1.86), Killip class >/=2 on admission (OR 2.30; 95% CI 1.29 to 4.09), LAVI >32 ml/m(2) (OR 2.22; 95% CI 1.25 to 3.96), diabetes (OR 1.94; 95% CI 1.15 to 3.28), and LV restrictive filling pattern (OR 1.89; 95% CI 1.09 to 3.31). CONCLUSIONS: In patients with acute MI, increased LA volume, determined within the first 48 h of admission, is an independent predictor of five-year mortality with incremental prognostic information to clinical and echocardiographic data.

Smoking increases inflammation and metalloproteinase expression in human carotid atherosclerotic plaques.

OBJECTIVES: To evaluate the effects of cigarette smoking on the composition of human carotid endarterectomy plaques. BACKGROUND: Smoking has been recognized as a major risk factor in atherogenesis. It is believed that smoking contributes to the atherosclerotic process and plaque instability in part by increasing the adherence of macrophages to the vessel wall and inducing the release of proteolytic enzymes. However, data are lacking in humans. METHODS: Carotid endarterectomy specimens of 21 smokers and 21 nonsmokers matched for age, gender, and symptoms were immunohistochemically stained with antibodies against CD68 (macrophages [MAC]), macrophage-derived metalloelastase (MMP-12), and tissue inhibitor of metalloproteinase 1 (TIMP-1). Sections were also evaluated for elastin content by van Gieson staining. The stained areas were planimetrically quantified as the percentage of immunopositive tissue area of the total tissue area. RESULTS: Smoking was associated with increased macrophage immunoreactivity (9.1% +/-7.4% vs 3.4% +/- 2.9%; P = .003) as well as increased expression of MMP-12 (13.4% +/- 6.7% vs 5.5% +/- 3.5%; P = .0004). However, plaques from smokers had decreased TIMP-1 expression (7.7% +/- 5.7% vs 13.1% +/- 8.5%; P = .04) and decreased elastin content (26.9% +/- 14.5% vs 38.9% +/- 18.4%; P = .02). CONCLUSIONS: This study demonstrates that cigarette smoking increases markers of inflammation and tissue destruction in atherosclerotic plaques. This change in plaque composition may at least in part explain the effect of smoking on the instability of human atherosclerotic plaques.

Acute myocardial infarction in human immunodeficiency virus-infected patients.

BACKGROUND: Patients infected with human immunodeficiency virus (HIV) are at an increased risk for premature coronary artery disease. However, the clinical outcome of HIV-infected patients who have had an acute myocardial infarction (AMI) is unknown. METHODS: We studied 24 consecutive HIV-infected patients admitted because of AMI. During the hospital phase, the patients were examined for recurrent ischemia, congestive heart failure, arrhythmia, and death. Patients were followed up for an average of 15 months after discharge for reinfarction; recurrent angina; the need for any angioplasty, bypass surgery, or target vessel revascularization for restenosis and stent thrombosis; HIV-related complications; and death. For comparison, we included a matched control group of non-HIV-infected patients. RESULTS: The HIV-infected patients with AMI were predominantly male (21 [88%]), 47 +/- 9 years of age. Twenty-two (92%) were receiving antiretroviral treatment; 17 (71%), protease inhibitors; and 13 (54%), lipid-lowering therapy. With aggressive therapy, the lipid profile was similar in HIV-infected patients treated with protease inhibitors and those who were not. Twenty-one (88%) of 24 patients underwent immediate angiography and 20 (83%) had angioplasty or bypass surgery. The HIV-infected patients with AMI had a benign in-hospital course, with no deaths or reinfarction. The admission characteristics, treatment strategy, and in-hospital outcome were similar in the matched uninfected patients with AMI. After discharge, HIV-infected patients had a higher incidence of reinfarction (4/20 [20%] vs 2/45 [4%]; P =.07), and 6 (43%) of 14 HIV-infected patients who had successful percutaneous coronary intervention and were available for follow-up required target vessel revascularization compared with 4 (11%) of 38 uninfected patients who had successful percutaneous coronary intervention and were available for follow-up (P =.02). CONCLUSIONS: Patients infected with HIV sustain AMI at a young age and have a benign in-hospital course. Although HIV-infected patients have a higher incidence of postdischarge ischemic events, restenosis, and stent thrombosis, the intermediate-term mortality is low.

Soluble intercellular adhesion molecule-1 and risk of future ischemic stroke: a nested case-control study from the Bezafibrate Infarction Prevention (BIP) study cohort.

BACKGROUND AND PURPOSE: Inflammation is considered to be involved in the pathogenesis of ischemic stroke. Our purpose was to assess the role of soluble intercellular adhesion molecule-1 (sICAM-1) concentration, a marker of inflammation, in predicting future ischemic stroke among patients at risk because of chronic coronary heart disease. METHODS: We obtained baseline serum samples from patients with chronic coronary heart disease enrolled in the Bezafibrate Infarction Prevention trial (n=3090), which assessed the efficacy of bezafibrate in secondary prevention. Using a prospective nested case-control design, we measured baseline sICAM-1 concentration in sera of patients who developed ischemic stroke during a mean follow-up of 8.2 years (cases, n=134) and in age- and sex-matched controls without any subsequent cardiovascular events (n=134). RESULTS: Baseline serum concentrations of sICAM-1 were significantly higher in cases compared with controls (379 versus 350 ng/mL, P<0.05). sICAM-1 concentration at the highest quartile (>394 ng/mL) was associated with significantly higher relative odds of ischemic stroke compared with the lower concentrations after adjustment for potential confounding variables (relative odds, 2.1; 95% CI, 1.1 to 4.3). After fibrinogen and total white blood cell count were added to the multivariable model, the relative odds were 2.1 (95% CI, 1.1 to 4.2) and 2.2 (95% CI, 1.1 to 4.8), respectively. The risk associated with raised concentrations of sICAM-1 seemed to be highest for large disabling strokes of cardioembolic origin. CONCLUSIONS: Elevated concentrations of sICAM-1, a marker of inflammation, are associated with increased risk of ischemic stroke, independent of other traditional cerebrovascular risk factors and of plasma fibrinogen, among patients at increased risk because of manifest coronary heart disease.

Timing of aspirin administration as a determinant of survival of patients with acute myocardial infarction treated with thrombolysis.

Unlike thrombolytic agents, there are conflicting data regarding the time-dependent effect of aspirin treatment on outcome in acute myocardial infarction (AMI). We sought to evaluate the impact of timing of aspirin administration (before vs after thrombolysis) on mortality of patients with AMI. Our study included 1,200 patients with ST elevation AMI treated with thrombolysis. Early (n = 364) versus late (n = 836) users were defined as those receiving emergency aspirin before versus after initiation of thrombolysis, respectively. Time (median) from symptom onset to initiation of aspirin treatment was significantly shorter in early versus late users (1.6 vs 3.5 hours; p <0.001). There were no significant differences between the 2 groups with respect to baseline clinical characteristics. Early aspirin users were more likely to develop reischemia, to be treated with beta blockers, to be referred to coronary angiography, percutaneous transluminal coronary angioplasty, or coronary artery bypass graft surgery. Early users experienced lower mortality at 7 days (2.5% vs 6.0%, p = 0.01), 30 days (3.3% vs 7.3%, p = 0.008), and 1 year (5.0% vs 10.6%, p = 0.002) than late users. This survival benefit persisted for patients with and without previous aspirin therapy or revascularization and after adjustment for baseline characteristics and therapies at 7 days (odds ratio 0.36, 95% confidence interval 0.15 to 0.79), at 30 days (odds ratio 0.39, 95% confidence interval 0.17 to 0.82), and at 1 year (odds ratio 0.41, 95% confidence interval 0.21 to 0.74). Our study proposes a time-dependent benefit from aspirin in patients with AMI treated with thrombolysis.