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Dive into the research topics where Andrew D. Michaels is active.

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Featured researches published by Andrew D. Michaels.


Circulation | 2011

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension A Scientific Statement From the American Heart Association

Michael R. Jaff; M. Sean McMurtry; Stephen L. Archer; Mary Cushman; Neil A. Goldenberg; Samuel Z. Goldhaber; J. Stephen Jenkins; Jeffrey A. Kline; Andrew D. Michaels; Patricia A. Thistlethwaite; Suresh Vedantham; R. James White; Brenda K. Zierler

Venous thromboembolism (VTE) is responsible for the hospitalization of >250 000 Americans annually and represents a significant risk for morbidity and mortality. Despite the publication of evidence-based clinical practice guidelines to aid in the management of VTE in its acute and chronic forms, the clinician is frequently confronted with manifestations of VTE for which data are sparse and optimal management is unclear. In particular, the optimal use of advanced therapies for acute VTE, including thrombolysis and catheter-based therapies, remains uncertain. This report addresses the management of massive and submassive pulmonary embolism (PE), iliofemoral deep vein thrombosis (IFDVT),and chronic thromboembolic pulmonary hypertension (CTEPH). The goal is to provide practical advice to enable the busy clinician to optimize the management of patients with these severe manifestations of VTE. Although this document makes recommendations for management, optimal medical decisions must incorporate other factors, including patient wishes, quality of life, and life expectancy based on age and comorbidities. The appropriateness of these recommendations for a specific patient may vary depending on these factors and will be best judged by the bedside clinician.


Circulation | 2002

Left Ventricular Systolic Unloading and Augmentation of Intracoronary Pressure and Doppler Flow During Enhanced External Counterpulsation

Andrew D. Michaels; Michel Accad; Thomas A. Ports; William Grossman

Background—Enhanced external counterpulsation (EECP) is a noninvasive, pneumatic technique that provides beneficial effects for patients with chronic, symptomatic angina pectoris. However, the physiological effects of EECP have not been studied directly. We examined intracoronary and left ventricular hemodynamics in the cardiac catheterization laboratory during EECP. Methods and Results—Ten patients referred for diagnostic evaluation underwent left heart catheterization and coronary angiography from the radial artery. At baseline and then during EECP, central aortic pressure, intracoronary pressure, and intracoronary Doppler flow velocity were measured using a coronary catheter, a sensor-tipped high-fidelity pressure guidewire, and a Doppler flow guidewire, respectively. Similar to changes in aortic pressure, EECP resulted in a dramatic increase in diastolic (71±10 mm Hg at baseline to 137±21 mm Hg during EECP; +93%;P <0.0001) and mean intracoronary pressures (88±9 to 102±16 mm Hg; +16%;P =0.006) with a decrease in systolic pressure (116±20 to 99±26 mm Hg; −15%;P =0.002). The intracoronary Doppler measure of average peak velocity increased from 11±5 cm/s at baseline to 23±5 cm/s during EECP (+109%;P =0.001). The TIMI frame count, a quantitative angiographic measure of coronary flow, showed a 28% increase in coronary flow during EECP compared with baseline (P =0.001). Conclusions—EECP unequivocally and significantly increases diastolic and mean pressures and reduces systolic pressure in the central aorta and the coronary artery. Coronary artery flow, determined by both Doppler and angiographic techniques, is increased during EECP. The combined effects of systolic unloading and increased coronary perfusion pressure provide evidence that EECP may serve as a potential mechanical assist device.


Circulation | 2005

Effects of Intravenous Levosimendan on Human Coronary Vasomotor Regulation, Left Ventricular Wall Stress, and Myocardial Oxygen Uptake

Andrew D. Michaels; Barry H. McKeown; Michael Kostal; Kalpesh T. Vakharia; Mark V. Jordan; Ivor L. Gerber; Elyse Foster; Kanu Chatterjee

Background—Levosimendan is a calcium-sensitizing agent and an inodilator under current investigation in the treatment of decompensated heart failure. The effects of intravenous levosimendan on the human coronary vasculature, together with myocardial wall stress and oxygen uptake, have not been adequately studied. Methods and Results—Ten adult patients underwent right- and left-heart catheterization. Baseline coronary blood flow was determined with quantitative coronary angiography and an intracoronary Doppler-tipped guidewire. Myocardial oxygen uptake was measured with a coronary sinus catheter. Echocardiography was performed before and 30 minutes after an intravenous infusion of levosimendan (24-&mgr;g/kg bolus over 10 minutes) was begun. Pulmonary capillary wedge decreased 37% (P=0.009), cardiac output increased 9% (P=0.04), and systemic vascular resistance decreased 18% (P<0.001). Left ventricular ejection fraction increased 20% (P=0.009), and meridional systolic wall stress decreased 48% (P=0.009). Coronary artery diameter increased 10% at 15 minutes (P=0.001) and 11% at 30 minutes (P=0.01). Coronary artery velocity increased 10% over baseline (P=0.04). Coronary blood flow increased 45% (P=0.02), whereas coronary resistance decreased 36% at 30 minutes (P=0.03). Myocardial oxygen extraction decreased 9% at 30 minutes (P=0.04). Conclusions—Levosimendan given intravenously exerts vasodilator effects on human coronary conductance and resistance arteries. Despite a decrease in coronary perfusion pressure, coronary blood flow is increased. A reduction in coronary vascular resistance and a decrease in coronary venous oxygen content indicate primary coronary vasodilation by levosimendan. Improved left ventricular systolic function and decreased myocardial oxygen extraction suggest improved myocardial efficiency.


Journal of the American College of Cardiology | 1998

Use of angiotensin-converting enzyme inhibitors at discharge in patients with acute myocardial infarction in the United States: data from the National Registry of Myocardial Infarction 2

Hal V. Barron; Andrew D. Michaels; Charles Maynard; Nathan R. Every

OBJECTIVES This study was undertaken to examine recent trends in the use of angiotensin-converting enzyme (ACE) inhibitor therapy in patients discharged after acute myocardial infarction (AMI) and to identify clinical factors associated with ACE inhibitor prescribing patterns. BACKGROUND Clinical trials have demonstrated a significant mortality benefit in patients treated with ACE inhibitors after AMI. Numerous studies have demonstrated underuse of other beneficial treatments for patients with AMI, such as beta-adrenergic blocking agents, aspirin and immediate reperfusion therapy. METHODS Demographic, procedural and discharge medication data from 190,015 patients with AMI were collected at 1,470 U.S. hospitals participating in the National Registry of Myocardial Infarction 2. RESULTS Prescriptions for ACE inhibitor therapy at hospital discharge increased from 25.0% in 1994 to 30.7% in 1996. Patients with a left ventricular ejection fraction < or =40% or evidence of congestive heart failure while in the hospital were discharged with ACE inhibitor treatment 42.6% of the time. Of patients experiencing an anterior wall myocardial infarction and no evidence of heart failure, 26.1% of patients were discharged with this treatment. Of the remaining patients, 15.6% received ACE inhibitors at discharge. ACE inhibitors were prescribed more often to elderly and diabetic patients as well as those requiring intraaortic balloon pump placement. This therapy was given less often to patients who underwent revascularization with coronary angioplasty or coronary artery bypass graft surgery or were treated with calcium channel blocking agents. CONCLUSIONS Physicians are prescribing ACE inhibitors in patients with myocardial infarction with increasing frequency. Those patients with the greatest expected benefit receive ACE inhibitor treatment most often. However, the majority of even these high risk patients were not discharged with this life-saving therapy.


Circulation | 2003

Effects of Intravenous Nesiritide on Human Coronary Vasomotor Regulation and Myocardial Oxygen Uptake

Andrew D. Michaels; Andrew Klein; James Madden; Kanu Chatterjee

Background—Nesiritide, recombinant human B-type natriuretic peptide, has been shown to be efficacious in the treatment of decompensated heart failure. The effects of intravenous nesiritide on the human coronary vasculature have not been studied. Methods and Results—Ten patients underwent right and left heart catheterization. Baseline coronary blood flow was determined using quantitative coronary angiography (QCA) and an intracoronary Doppler-tipped guidewire. Myocardial oxygen uptake was measured using a coronary sinus catheter. Patients then received an intravenous infusion of nesiritide (2 &mgr;g/kg bolus followed by 0.01 &mgr;g/kg per min infusion) for 30 minutes. Right atrial pressure decreased 52% (P =0.012), pulmonary artery mean pressure decreased 19% (P =0.03), pulmonary capillary wedge pressure decreased 46% (P =0.002), and mean arterial pressure decreased 11% (P =0.007). QCA demonstrated a 15% increase in coronary artery diameter from a baseline of 2.6±0.8 to 3.0±0.8 mm at 30 minutes (P =0.007). The coronary velocity measure of average peak velocity increased 14% from 20.8±6.4 at baseline to 23.8±7.2 cm/s at 5 minutes (P =0.015) and then returned to baseline for the remainder of the infusion. Coronary blood flow increased 35% (P =0.007), whereas coronary resistance decreased 23% at 15 and 30 minutes (P =0.036). Myocardial oxygen uptake decreased 8% during the nesiritide infusion (P =0.043). Conclusions—Nesiritide exerts coronary vasodilator effects on both the coronary conductance and resistance arteries. Despite a decrease in coronary perfusion pressure, coronary artery blood flow is increased, coronary resistance is decreased, and myocardial oxygen uptake is decreased.


Clinical Cardiology | 2008

Enhanced External Counterpulsation in the Treatment of Chronic Refractory Angina: A Long-term Follow-up Outcome from the International Enhanced External Counterpulsation Patient Registry

P.H. Loh; John G.F. Cleland; Amal A. Louis; Elizabeth D. Kennard; Jocelyn F. Cook; John L. Caplin; Gregory W. Barsness; William Lawson; Ozlem Soran; Andrew D. Michaels

The management of patients who suffer from medically refractory angina and are unsuitable for conventional revascularization therapy is often unsatisfactory. Enhanced external counterpulsation (EECP) is a noninvasive treatment that is safe and effective immediately after a course of treatment. However, the duration of benefit is less certain.


Circulation | 2010

Medication Errors in Acute Cardiovascular and Stroke Patients A Scientific Statement From the American Heart Association

Andrew D. Michaels; Sarah A. Spinler; Barbara Leeper; E. Magnus Ohman; Karen P. Alexander; L. Kristin Newby; Hakan Ay; W. Brian Gibler

Medical errors are the eighth leading cause of death in the United States and are estimated to account for somewhere between 44 000 and 98 000 deaths in the United States each year.1 An exact number of deaths remains both uncertain and controversial, with arguments that the actual figure may be lower2 or higher.3 Each year in the United States, the estimated 450 000 preventable medication-related adverse events cost


Journal of Electrocardiology | 2009

Intravenous electrocardiographic guidance for placement of peripherally inserted central catheters

Brigham Smith; Renée M. Neuharth; Mary Ann Hendrix; Daniel McDonnall; Andrew D. Michaels

3.5 billion.4 In the Health Grades Inc Patient Safety in American Hospitals study, which examined 37 million patient records, it was estimated that 195 000 Medicare patients die due to preventable, in-hospital medical errors annually.3 Medication errors are the most common type of medical error, and cardiovascular medications prescribed to inpatients account for a large proportion of these errors. An average of 1 medication error occurs per hospitalized patient per day, and one quarter of all medication-related injuries are preventable. The emergency department (ED) and acute hospital setting remain locations at high risk for medication errors. Since the Institute of Medicine’s 2000 report, “To Err Is Human: Building a Safer Health System,” there has been heightened awareness of medical and medication errors.1 In 2001, Congress appropriated


Circulation | 2002

Angioplasty Versus Bypass Surgery for Coronary Artery Disease

Andrew D. Michaels; Kanu Chatterjee

50 million for major initiatives in patient safety and directed the Agency for Healthcare Research and Quality to establish the Center for Quality Improvement and Patient Safety. The following year, the American Heart Association (AHA) issued its first scientific statement on medication errors in acute cardiac care.5 In 2003, Congress passed the Medicine Modernization Act to charge the Institute of Medicine with formulating a national agenda aimed at reducing medication errors. In these early years after the Institute of Medicine’s report, the topic of patient safety became a frequent focus for healthcare leaders, journalists, and concerned citizens. Although …


Catheterization and Cardiovascular Interventions | 2007

Determination of adequate coronary stent expansion using StentBoost, a novel fluoroscopic image processing technique.

Jacob Mishell; Kalpesh T. Vakharia; Thomas A. Ports; Yerem Yeghiazarians; Andrew D. Michaels

BACKGROUND Correct positioning of peripherally inserted central catheters (PICCs) is essential to avoid complications. We evaluated intravenous electrocardiogram (ECG) recordings during PICC placement to assess the effectiveness of this guidance technique to reduce complications resulting from incorrect catheter placement. METHODS Six patients undergoing PowerPICC catheter insertion were included in this pilot study. Venography through the PICC was performed to identify the superior vena cava-right atrial (SVC-RA) junction. Unipolar ECG recordings from the catheter stylet measured P-wave changes during PICC insertion. RESULTS The peak P-wave amplitude was highest at the SVC-RA junction. With catheter insertion into the RA, P-wave amplitude decreased and eventually became negative. With catheter withdrawal into the SVC, P-wave amplitude decreased. CONCLUSIONS P-wave amplitude was highest when the PICC catheter was in the optimal location at the SVC-RA junction. Intravenous ECG monitoring during PICC insertion seems to be a promising technique to guide catheter positioning.

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Elyse Foster

University of California

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Mark V. Jordan

University of California

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Ozlem Soran

University of Pittsburgh

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