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1.  Impact of main branch stenting on endothelial shear stress: role of side branch diameter, angle and lesion 
In-stent restenosis and stent thrombosis remain clinically significant problems for bifurcation lesions. The objective of this study is to determine the haemodynamic effect of the side branch (SB) on main branch (MB) stenting. We hypothesize that the presence of a SB has a negative effect on MB wall shear stress (WSS), wall shear stress gradient (WSSG) and oscillatory shear index (OSI); and that the bifurcation diameter ratio (SB diameter/MB diameter) and angle are important contributors. We further hypothesized that stent undersizing exaggerates the negative effects on WSS, WSSG and OSI. To test these hypotheses, we developed computational models of stents and non-Newtonian blood. The models were then interfaced, meshed and solved in a validated finite-element package. Stents at bifurcation models were created with 30° and 70° bifurcation angles and bifurcations with diameter ratios of SB/MB = 1/2 and 3/4. It was found that stents placed in the MB at a bifurcation lowered WSS dramatically, while elevating WSSG and OSI. Undersizing the stent exaggerated the decrease in WSS, increase in WSSG and OSI, and disturbed the flow between the struts and the vessel wall. Stenting the MB at bifurcations with larger SB/MB ratios or smaller SB angles (30°) resulted in lower WSS, higher WSSG and OSI. Stenosis at the SB lowered WSS and elevated WSSG and OSI. These findings highlight the effects of major biomechanical factors in MB stenting on endothelial WSS, WSSG, OSI and suggests potential mechanisms for the potentially higher adverse clinical events associated with bifurcation stenting.
doi:10.1098/rsif.2011.0675
PMCID: PMC3350730  PMID: 22112654
bifurcation stents; endothelial shear stress; stent sizing; provisional stenting; incomplete apposition
2.  Intramyocardial, Autologous CD34+ Cell Therapy for Refractory Angina 
Circulation research  2011;109(4):428-436.
Rationale
A growing number of patients with coronary disease have refractory angina. Preclinical and early-phase clinical data suggest that intramyocardial injection of autologous CD34+ cells can improve myocardial perfusion and function.
Objective
Evaluate the safety and bioactivity of intramyocardial injections of autologous CD34+ cells in patients with refractory angina who have exhausted all other treatment options.
Methods and Results
In this prospective, double-blind, randomized, phase II study (ClinicalTrials.gov identifier: NCT00300053), 167 patients with refractory angina received 1 of 2 doses (1×105 or 5×105 cells/kg) of mobilized autologous CD34+ cells or an equal volume of diluent (placebo). Treatment was distributed into 10 sites of ischemic, viable myocardium with a NOGA mapping injection catheter. The primary outcome measure was weekly angina frequency 6 months after treatment. Weekly angina frequency was significantly lower in the low-dose group than in placebo-treated patients at both 6 months (6.8±1.1 versus 10.9±1.2, P=0.020) and 12 months (6.3±1.2 versus 11.0±1.2, P=0.035); measurements in the high-dose group were also lower, but not significantly. Similarly, improvement in exercise tolerance was significantly greater in low-dose patients than in placebo-treated patients (6 months: 139±151 versus 69±122 seconds, P=0.014; 12 months: 140±171 versus 58±146 seconds, P=0.017) and greater, but not significantly, in the high-dose group. During cell mobilization and collection, 4.6% of patients had cardiac enzyme elevations consistent with non-ST segment elevation myocardial infarction. Mortality at 12 months was 5.4% in the placebo-treatment group with no deaths among cell-treated patients.
Conclusions
Patients with refractory angina who received intramyocardial injections of autologous CD34+ cells (105 cells/kg) experienced significant improvements in angina frequency and exercise tolerance. The cell-mobilization and -collection procedures were associated with cardiac enzyme elevations, which will be addressed in future studies.
doi:10.1161/CIRCRESAHA.111.245993
PMCID: PMC3190575  PMID: 21737787
angiogenesis; endothelial progenitor cells (EPC) myocardial ischemia; myocardial regeneration; stem cells
3.  Two Mechanistic Pathways for Thienopyridine-Associated Thrombotic Thrombocytopenic Purpura 
Objectives
We sought to describe clinical and laboratory findings for a large cohort of patients with thienopyridine-associated thrombotic thrombocytopenic purpura (TTP).
Background
The thienopyridine derivatives, ticlopidine and clopidogrel, are the 2 most common drugs associated with TTP in databases maintained by the U.S. Food and Drug Administration (FDA).
Methods
Clinical reports of TTP associated with clopidogrel and ticlopidine were identified from medical records, published case reports, and FDA case reports (n = 128). Duration of thienopyridine exposure, clinical and laboratory findings, and survival were recorded. ADAMTS13 activity (n = 39) and inhibitor (n = 30) were measured for a subset of individuals.
Results
Compared with clopidogrel-associated TTP cases (n = 35), ticlopidine-associated TTP cases (n = 93) were more likely to have received more than 2 weeks of drug (90% vs. 26%), to be severely thrombocytopenic (84% vs. 60%), and to have normal renal function (72% vs. 45%) (p < 0.01 for each). Compared with TTP patients with ADAMTS13 activity >15% (n = 13), TTP patients with severely deficient ADAMTS13 activity (n = 26) were more likely to have received ticlopidine (92.3% vs. 46.2%, p < 0.003). Among patients who developed TTP >2 weeks after thienopyridine, therapeutic plasma exchange (TPE) increased likelihood of survival (84% vs. 38%, p < 0.05). Among patients who developed TTP within 2 weeks of starting thienopyridines, survival was 77% with TPE and 78% without.
Conclusions
Thrombotic thrombocytopenic purpura is a rare complication of thienopyridine treatment. This drug toxicity appears to occur by 2 different mechanistic pathways, characterized primarily by time of onset before versus after 2 weeks of thienopyridine administration. If TTP occurs after 2 weeks of ticlopidine or clopidogrel therapy, therapeutic plasma exchange must be promptly instituted to enhance likelihood of survival.
doi:10.1016/j.jacc.2007.04.093
PMCID: PMC3167088  PMID: 17868804
4.  Drug-Eluting Stents versus Bare Metal Stents in Unprotected Left Main Coronary Artery Stenosis: a Meta-Analysis 
Objectives
We undertook a meta-analysis to assess outcomes for drug-eluting (DES) and bare metal stents (BMS) in percutaneous coronary intervention (PCI) for unprotected left main coronary stenosis (LMCA).
Background
Uncertainty exits regarding the relative performance of DES versus BMS in unprotected LMCA PCI.
Methods
Of a total of 838 studies, 44 met inclusion criteria (N=10,342). The co-primary endpoints were mortality, myocardial infarction (MI), target vessel/target lesion revascularization (TVR/TLR), and major adverse cardiac events (MACE: mortality, MI, TVR/TLR).
Results
Event rates for DES and BMS were calculated at 6–12 months, at 2 years and at 3 years. Crude event rates at 3 years were: mortality (8.8% and 12.7%), MI (4.0% and 3.4%), TVR/TLR (8.0% and 16.4%), and MACE (21.4% and 31.6%). Nine studies were included in a comparative analysis (N=5,081). At 6–12 months the adjusted odds ratio (OR) for DES vs. BMS were: mortality 0.94 (95% confidence interval [CI] 0.06–15.48; p=0.97), MI 0.64 (95% CI 0.19–2.17; p=0.47), TVR/TLR 0.10 (95% CI 0.01–0.84; p=0.01) and MACE 0.34 (95% CI 0.15–0.78; p=0.01). At 2 years the OR were: mortality 0.42 (95% CI 0.28–0.62; p<0.01), MI 0.16 (95% CI 0.01–3.53; p=0.13), and MACE 0.31 (95% CI 0.15–0.66; p<0.01). At 3 years the OR were: mortality 0.70 (95% CI 0.53–0.92; p=0.01), MI 0.49 (95% CI 0.26–0.92; p=0.03), TVR/TLR 0.46 (95% CI 0.30–0.69; p<0.01), and MACE 0.78 (95% CI 0.57–1.07; p=0.12).
Conclusion
Our meta-analysis suggests that DES is associated with favorable outcomes for mortality, MI, TVR/TLR, and MACE as compared to BMS in unprotected LMCA PCI.
doi:10.1016/j.jcin.2010.03.019
PMCID: PMC3072800  PMID: 20630453
5.  Multiple myeloma presenting with high-output heart failure and improving with anti-angiogenesis therapy: two case reports and a review of the literature 
Introduction
Common manifestations of multiple myeloma include osteolytic lesions, cytopenias, hypercalcemia, and renal insufficiency. Patients may also exhibit heart failure which is often associated with either past therapy or cardiac amyloidosis. A less recognized mechanism is high-output heart failure. Diuretic therapy in this setting has little efficacy in treating the congested state. Furthermore, effective pharmacotherapy has not been established. We report two patients with multiple myeloma and high-output heart failure who failed diuretic therapy. The patients were given dexamethasone in conjunction with lenalidomide and thalidomide, respectively. Shortly thereafter, each patient demonstrated a significant improvement in symptoms. This is the first report of successful treatment of multiple myeloma-induced high-output failure via the utilization of these agents.
Case presentation
Two patients with multiple myeloma were evaluated for volume overload. The first was a 50-year-old man with refractory disease. Magnetic resonance imaging demonstrated diffuse marrow replacement throughout the pelvis. Cardiac catheterization conveyed elevated filling pressures and a cardiac output of 15 liters/minute. He quickly decompensated and required mechanical ventilation. The second patient was a 61-year-old man recently diagnosed with multiple myeloma and volume overload. Skeletal survey demonstrated numerous lytic lesions throughout the pelvis. His cardiac catheterization also conveyed elevated filling pressures and a cardiac output of 10 liters/minute. Neither patient responded to diuretic therapy and they were subsequently started on dexamethasone plus lenalidomide and thalidomide, respectively. The first patient's brisk diuresis allowed for extubation within 48 hours after the first dose. He had a net negative fluid balance of 15 liters over 10 days. The second patient also quickly diuresed and on repeat cardiac catheterization, his cardiac output had normalized to 4.7 liters/minute.
Conclusion
Multiple myeloma can cause high-output failure. The mechanism is likely extensive bony involvement causing innumerable intramedullary arteriovenous fistulas. Diuretic therapy is not effective in treating this condition. Lenalidomide and thalidomide, both of which inhibit angiogenesis, seem to be viable treatment options. Based on the rapid and effective results seen in these two patients, a potential novel mechanism of 'pharmacologic fistula ligation' with these agents may be the most effective way to treat this presentation.
doi:10.1186/1752-1947-2-229
PMCID: PMC2500028  PMID: 18627621
6.  Accelerating restrictive cardiomyopathy after liver transplantation in a patient with familial amyloidotic polyneuropathy: a case report 
Introduction
Hereditary amyloidodis is a rare disease process with a propensity to cause polyneuropathies, autonomic dysfunction, and restrictive cardiomyopathy. It is transmitted in an autosomal dominant manner, with disease onset usually in the 20s-40s. The most common hereditary amyloidogenic protein, transthyretin, is synthesized in the liver and lies on Chromosome 18. Over 80 amyloidogenic transthyretin mutations have been described, the majority of which are neuropathic and hence the common name, Familial Amyloidotic Polyneuropathy. Until 1990, the disease was intractable with a 5–15 year survival after diagnosis. The prognosis changed after the implementation of orthotropic liver transplantation as a treatment strategy which halts the synthesis of amyloidogenic transthyretin. This has now has been performed over 1300 times in 67 centers.
Case presentation
We describe the case of a man of Irish ancestry with Familial Amyloidotic Polyneuropathy and no clinical history of cardiac involvement. Shortly after orthotropic liver transplantation, he developed congestive heart failure. He was subsequently diagnosed with an accelerating post-transplant restrictive cardiomyopathy due to amyloid infiltration.
Conclusion
A liver transplant induced cardiomyopathy in Familial Amyloidotic Polyneuropathy can be observed in patients without any history of cardiac symptoms. All patients with Familial Amyloidotic Polyneuropathy should be followed after transplantation to assess for a deterioration in cardiac function.
doi:10.1186/1752-1947-2-35
PMCID: PMC2248590  PMID: 18241340
7.  Percutaneous coronary intervention in a patient with cardiac dextroversion 
Dextrocardia associated with atrial situs solitus is commonly referred to as dextroversion. Dextroversion is a result of early interruption of normal embryological development and, therefore, rarely occurs without other associated cardiac and noncardiac anomalies. While percutaneous coronary intervention has been described in many cases of dextrocardia with situs inversus, it has not been previously described in dextroversion. We report the case of an 88-year-old woman with dextroversion who presented with an acute anterior myocardial infarction that was successfully treated with coronary stent implantation.
PMCID: PMC1484529  PMID: 17252039
8.  Method for Sampling Beef Carcasses 
An instrument resembling a surgical dermatome, for microbiological sampling of beef carcasses, is described.
Images
PMCID: PMC242928  PMID: 16345292
9.  Medium for the Selective Enumeration of Lactic Acid Bacteria from Foods 
Applied Microbiology  1973;26(3):439-440.
A nitrite actidione polymyxin agar was developed for the enumeration of lactic acid bacteria. It was effective in recovering organisms from pure cultures and from foods.
PMCID: PMC379813  PMID: 4356465

Results 1-25 (37)