Cardiovascular system and COVID-19: manifestations and therapeutics.

The world is currently in the midst of a daunting global pandemic due to SARS-CoV-2 viral infection and associated COVID-19 disease. Healthcare professionals are tasked with the challenge of managing diverse multisystem clinical manifestations of this infection. Although acute hypoxic respiratory failure is the hallmark of severe COVID-19 disease, there have been diverse manifestations within the cardiovascular (CV) system that each pose unique therapeutic challenges. Of these manifestations, myocardial injury and right ventricular dysfunction are the most common, however, heart failure, circulatory shock, cardiomyopathy, arrhythmia, and vascular thrombosis have been noted as well. Furthermore, these CV related manifestations portend greater morbidity and mortality, which requires clinicians to be familiar with the most recent information to provide informed patient care. Although there are limited treatment options available for COVID-19, it is imperative that the potential cardiovascular implications of these therapies are considered in these patients. This review highlights the pathophysiological mechanisms of and therapeutics for CV manifestations of COVID-19 as well as the CV implications of proposed COVID-19 therapies. Since our hospital-based providers are the frontline caregivers battling this pandemic, the aim of this review is to assist with clinical decision-making for optimal patient outcomes while maintaining a safe environment for healthcare personnel.

High-Grade Spindle Cell Sarcoma of the Heart: A Rare Cause of Mitral Valve Disease.

A young female with pulmonary congestion suspected to be secondary to mitral valve disease with left atrial appendage thrombus was given therapy for heart failure and anticoagulation. Subsequent multimodality imaging with echocardiography and magnetic resonance imaging established an accurate but rare diagnosis of spindle cell sarcoma of the heart. (Level of Difficulty: Intermediate.).

Noninvasive imaging techniques of constrictive pericarditis.

Constrictive pericarditis (CP) is the result of scarring and loss of elasticity of the pericardial sac, resulting in external impedance of cardiac filling. It can occur after virtually any pericardial disease process. Patients typically present with signs and symptoms of right heart failure and/or low cardiac output. An important pathophysiological hallmark of CP is exaggerated ventricular interdependence and impaired diastolic filling. Echocardiography is the initial imaging modality for diagnosis of CP. Unfortunately, no echocardiographic sign or combination of signs is pathognomonic for CP. CT scan and cardiac MRI are other imaging techniques that can provide incremental diagnostic information. CT scan can easily detect pericardial thickening and calcification, while cardiac MRI provides a comprehensive evaluation of the pericardium, myocardium and cardiac physiology. Occasionally, a multimodality approach needs to be considered for the conclusive diagnosis of CP.

Segmental wall-motion abnormalities of the left ventricle predict arrhythmic events in patients with nonischemic cardiomyopathy.

BACKGROUND: Nonischemic dilated cardiomyopathy (NICM) is associated with diffuse global hypokinesia on echocardiography. However, NICM also may be associated with segmental wall-motion abnormalities (SWMAs) even in the presence of global hypokinesia, probably secondary to patchy myocardial scars. OBJECTIVE: Because myocardial scars serve as substrate for reentry, the purpose of this study was to determine whether SWMA is a predictor of ventricular arrhythmic events in NICM. METHODS: Echocardiographic parameters and appropriate implantable cardioverter-defibrillator (ICD) therapy for arrhythmic events (shock or antitachycardia pacing) were studied in NICM patients with an ICD. Two-dimensional echocardiography of the left ventricle was recorded in a 16-segment model. SWMA was defined by the presence of akinesia or moderate to severe hypokinesia in at least two segments. Patients were divided into one of two groups according to the presence (SWMA group) or the absence (non-SMWA group) of SWMA. RESULTS: SWMA was present in 47.5% of 101 patients (mean age 58.0 ± 15.6 years, 85% male, primary prophylaxis indication 46%, mean ejection fraction 26% ± 9%, mean follow-up 29 ± 18.4 months) studied. No significant difference in mean age, ejection fraction, and QRS duration was seen between SWMA and non-SWMA groups. The SWMA group had a significantly higher incidence of arrhythmic events than did the non-SWMA group (65% vs 15%, P <.001). Kaplan-Meier survival analysis revealed that SMWA was associated with significantly reduced time to first arrhythmic event (P = .001). SWMA (P <0.001), New York Heart Association heart failure class (P = .016), and secondary prevention indication for ICD placement (P = .005) were significant independent predictors of an arrhythmic event. SWMA did not predict mortality. CONCLUSION: SWMA is an independent predictor of arrhythmic events in patients with NICM.

Current noninvasive imaging techniques for detection of coronary artery disease.

The development and widespread use of noninvasive imaging techniques have contributed to the improvement in evaluation of patients with known or suspected coronary artery disease. Stress echocardiography and single-photon computed tomography are well-established noninvasive techniques with a proven track record for the diagnosis of coronary atherosclerosis. These modalities are generally widely available and provide a relatively high sensitivity and specificity along with an incremental value over clinical risk factors for detection of coronary artery disease. PET has a high diagnostic performance but continues to have limited clinical use because of the high expense of the dedicated equipment and difficulties in obtaining adequate radionuclides. Cardiac MRI and multislice computed tomography constitute the most recent addition to the cardiac imaging armamentarium. Cardiac MRI offers a comprehensive cardiac evaluation, which includes wall-motion analysis, myocardial tissue morphology, rest and stress first-pass myocardial perfusion, as well as ventricular systolic function. Cardiac computed tomography allows coronary calcium scanning along with noninvasive anatomic assessment of the coronary tree. It can be combined with functional imaging to provide a complete evaluation of the presence and physiological significance of the atherosclerotic coronary disease. No single imaging modality has been proven to be superior overall. Available tests all have advantages and drawbacks, and none can be considered suitable for all patients. The choice of the imaging method should be tailored to each person based on the clinical judgment of the a priori risk of cardiac event, clinical history and local expertise.

Usefulness of fragmented QRS on a 12-lead electrocardiogram in acute coronary syndrome for predicting mortality.

Electrocardiographic signs of a non-ST elevation myocardial infarction (NSTEMI) are nonspecific, and therefore the diagnosis of NSTEMI during acute coronary syndromes (ACS) depends mainly on cardiac biomarker levels. Fragmented QRS (fQRS) represents myocardial conduction abnormalities due to myocardial infarction (MI) scars in patients with coronary artery disease. However, the time of appearance of fQRS during ACS has not been investigated. It was postulated that in patients with ACS, fQRS on 12-lead electrocardiography occurs within 48 hours of presentation with NSTEMI as well as ST elevation MI and that fQRS predicts mortality. Serial electrocardiograms from 896 patients with ACS (mean age 62 +/- 11 years, 98% men) who underwent cardiac catheterization were studied. Four hundred forty-one patients had MIs, including 337 patients with NSTEMIs, and 455 patients had unstable angina (the control group). Serial electrocardiograms were obtained every 6 to 8 hours during the first 24 hours after the diagnosis of MI and the next day (<48 hours). Fragmented QRS on 12-lead electrocardiography was defined by the presence of single or multiple notches in the R or S wave, without a typical bundle branch block, in > or =2 contiguous leads in 1 of the major coronary artery territories. Fragmented QRS developed in 224 patients (51%) in the MI group and only 17 (3.7%) in the control group (p <0.001). New Q waves developed in 122 (28%), 76 (23%), and 2 (0.4%) patients in the MI, NSTEMI, and control groups, respectively. The sensitivity values of fQRS for ST elevation MI and NSTEMI were 55% and 50%, respectively. The specificity of fQRS was 96%. Kaplan-Meier survival analysis revealed that patients with fQRS had significantly decreased times to death compared to those without fQRS. Fragmented QRS, T-wave inversion, and ST depression were independent predictors of mortality during a mean follow-up period of 34 +/- 16 months. In conclusion, fQRS on 12-lead electrocardiography is a moderately sensitive but highly specific sign for ST elevation MI and NSTEMI. Fragmented QRS is an independent predictor of mortality in patients with ACS.

Fragmented QRS complexes on 12-lead ECG: a marker of cardiac sarcoidosis as detected by gadolinium cardiac magnetic resonance imaging.

BACKGROUND: Fragmented QRS complexes (fQRS) on a 12-lead ECG are a marker of myocardial scar in patients with coronary artery disease. Cardiac sarcoidosis is also associated with myocardial granuloma formation and scarring. We evaluated the significance of fQRS on a 12-lead ECG compared to Gadolinium-delayed enhancement images (GDE) in cardiac magnetic resonance imaging (CMR). METHOD AND RESULTS: The ECGs of patients (n = 17, mean age: 52 +/- 11 years, male: 53%) with established diagnosis of sarcoidosis who underwent a CMR for evaluation of cardiac involvement were studied. ECG abnormalities included bundle branch block, Q wave, and fQRS. fQRS, Q wave, and bundle branch block were present in 9 (53%), 1 (6%), and 4 (24%) patients, respectively. The sensitivity and specificity of fQRS for detecting abnormal GDE were 100% and 80%, respectively. Sensitivity and specificity of Q waves were 11% and 100%, respectively. CONCLUSIONS: fQRS on a 12-lead ECG in patients with suspected cardiac sarcoidosis are associated with cardiac involvement as detected by GDE on CMR.

Perioperative risk predictors of cardiac outcomes in patients undergoing liver transplantation surgery.

BACKGROUND: Cardiac risk assessment for perioperative outcomes of liver transplantation patients is limited. We examined the outcomes of an older intermediate-cardiac-risk group of patients undergoing liver transplantation surgery. METHODS AND RESULTS: Patients who had liver transplantation surgery between 2001 and 2005 were studied. The 3 outcomes analyzed were nonfatal myocardial infarction, death, and either outcome within the first 30 days after the liver transplantation surgery. Of 403 patients (mean age, 52+/-9 years; 67% male), 106 (26%) were diabetic, 84 (21%) were hypertensive, and 173 (43%) had a history of smoking. There were 48 total events (12%), 25 myocardial infarctions (7%), and 38 deaths (9%) recorded during the perioperative period. From the final multivariate model, history of coronary artery disease, prior stroke, and postoperative sepsis predicted greater risk (P=0.014; odds ratio [OR], 4.0; 95% confidence interval [CI], 1.3 to 11.8; P=0.025; OR, 6.6; 95% CI, 1.3 to 33.8; and P<0.001; OR, 7.5; 95% CI, 3.3 to 17.1, respectively). Use of perioperative beta-blockers was protective (P=0.004; OR, 0.20; 95% CI, 0.1 to 0.6) for combined cardiac outcomes. For the outcome of death on multivariate analysis, postoperative sepsis and increased interventricular septal thickness predicted risk (P<0.001; OR, 8.6; 95% CI, 3.5 to 20.9; and P=0.027; OR, 2.8; 95% CI, 1.1 to 7.2, respectively), whereas the use of perioperative beta-blockers was again protective (P=0.012; OR, 0.07; 95% CI, 0.01 to 0.56). CONCLUSIONS: In our study of cardiac risk assessment for liver transplantation surgery, history of stroke, coronary artery disease, postoperative sepsis, and increased interventricular septal thickness were markers of adverse perioperative cardiac outcomes, whereas use of perioperative beta-blockers was significantly protective.

Inflammatory aortitis with coronary arterial involvement by multidetector cardiac computed tomography.

A 40-year-old man with a history of hypertension was admitted for a non-ST-segment myocardial infarction. A multidetector coronary computed tomography (MDCCT) showed proximal aortic intramural thickening with extrinsic thickening and luminal compression of the proximal left circumflex coronary artery. Subsequent surgical evaluation and positron emission tomography imaging showed evidence of active inflammation of the proximal aorta and coronary arteries. Hence, this case illustrates an uncommon cause of myocardial ischemia and the emerging complimentary role that MDCCT can play in such patients.

A hazardous finding of a rare anomalous left main coronary artery in a patient with a secundum atrial septal defect.

A 23-year-old male referred for evaluation of a "choking" sensation with exertion and a murmur. A transthoracic echocardiogram demonstrated right atrial and ventricular dilatation, right ventricular volume overload, and a large secundum atrial septal defect (ASD) with left to right shunt and a calculated pulmonary-to-systemic blood flow ratio (Qp/Qs) estimated at 2.3 to 1. Cardiac catheterization also demonstrated evidence of the ASD with Qp/Qs of 4.6 to 1 with a significant step-up in oxygen saturation at the right atrial level. Additionally, an anomalous left main coronary artery (ALMCA) origin from the anterior right coronary cusp was suspected. Using 64-slice multidetector computed tomography coronary angiography (CCTA) the left main coronary artery was seen to arise from the right coronary cusp then traverse between the pulmonary trunk and the proximal ascending aorta before bifurcating into the left anterior descending and circumflex arteries that followed their normal courses distally. Based on the high risk nature of associated sudden death from an anomalous left main coronary artery (ALMCA) coursing between the aorta and the pulmonary trunk, the patient underwent surgical re-implantation of the ALMCA to the left coronary cusp and repair of the ASD. This case highlights a rare finding of a hazardous ALMCA in a patient with a secundum ASD and the utility of CCTA in evaluating the course of coronary anomalies along with other cardiac pathology.

Fragmented wide QRS on a 12-lead ECG: a sign of myocardial scar and poor prognosis.

BACKGROUND: Fragmented QRS (duration <120 ms) on a 12-lead ECG represents myocardial scar in patients with coronary artery disease. However, the significance of fragmented QRS has not been defined in the presence of a wide QRS (wQRS; duration >or=120 ms). We postulate that fragmented wQRS (f-wQRS) due to bundle branch block, premature ventricular complexes, or paced rhythms (f-pQRS) signify myocardial scar and higher mortality. METHODS AND RESULTS: Patients who underwent cardiac evaluation with nuclear stress imaging or cardiac catheterization and had wQRS (bundle branch block, premature ventricular complex, or pQRS) were studied. f-wQRS was defined by the presence of >2 notches on the R wave or the S wave and had to be present in >or=2 contiguous inferior (II, III, aVF), lateral (I, aVL, V(6)) or anterior (V(1) to V(5)) leads. ECG analyses of 879 patients (age, 66.7+/-11.4 years; male, 97%; mean follow-up, 29+/-18 months) with bundle branch block (n=310), premature ventricular complex (n=301), and pQRS (n=268) revealed f-wQRS in 415 (47.2%) patients. Myocardial scar was present in 440 (50%) patients. The sensitivity, specificity, positive predictive value, and negative predictive value of f-wQRS for myocardial scar were 86.8%, 92.5%, 92.0%, and 87.5%, respectively. The sensitivity and specificity for diagnosing myocardial scar were 88.6% and 94.4%, 81.4% and 88.4%, and 89.8% and 95.7% for f-bundle branch block, f-premature ventricular complex, and f-pQRS, respectively. f-wQRS was associated with mortality after adjusting for age, ejection fraction, and diabetes (P=0.017). CONCLUSIONS: f-wQRS on a standard 12-lead ECG is a moderately sensitive and highly specific sign for myocardial scar in patients with known or suspected coronary artery disease. f-wQRS is also an independent predictor of mortality.

Fragmented QRS on a 12-lead ECG: a predictor of mortality and cardiac events in patients with coronary artery disease.

BACKGROUND: Fragmented QRS (fQRS) on a 12-lead electrocardiogram (ECG) is associated with myocardial scar in patients with coronary artery disease (CAD). OBJECTIVE: We postulated that fQRS is a predictor of cardiac events and mortality in patients who have known CAD or who are being evaluated for CAD. METHODS: The cardiac events (myocardial infarction, need for revascularization, or cardiac death) and all-cause mortality were retrospectively reviewed in 998 patients (mean age 65.5 +/- 11.9 years, male 967) who underwent nuclear stress test. The fQRS on a 12-lead ECG included various RSR' patterns (> or =1 R' prime or notching of S wave or R wave) without typical bundle branch block in 2 contiguous leads corresponding to a major coronary artery territory. RESULTS: All-cause mortality (93 [34.1%] vs 188 [25.9%]) and cardiac event rate (135 [49.5%] vs 200 [27.6%]) were higher in the fQRS group compared with the non-fQRS group during a mean follow-up of 57 +/- 23 months. A Kaplan-Meier survival analysis revealed significantly lower event-free survival for cardiac events (P <.001) and all-cause mortality (P = .02). Multivariate Cox regression analysis revealed that significant fQRS was an independent significant predictor for cardiac events but not for all-cause mortality. The Kaplan-Meier survival analysis showed no significant difference between fQRS and Q waves groups for cardiac events (P = .48) and all-cause mortality (P = .08). CONCLUSION: The fQRS is an independent predictor of cardiac events in patients with CAD. It is associated with significantly lower event-free survival for a cardiac event on long-term follow-up.

Fragmented QRS complexes not typical of a bundle branch block: a marker of greater myocardial perfusion tomography abnormalities in coronary artery disease.

BACKGROUND: Fragmented QRS (FQRS) complexes, not typical of a bundle branch block, are a marker of regional myocardial injury. The extent of stress myocardial perfusion imaging (MPI) abnormalities with FQRS patterns is not known. METHODS AND RESULTS: Twelve-lead electrocardiograms (ECGs) in 501 patients undergoing stress MPI were studied. FQRS was defined as a QRS duration of 120 milliseconds or less, with notches or slurs of QRS complexes, on 2 contiguous leads of a coronary artery territory. Abnormal MPI was defined as a regional summed stress score (SSS) and summed rest score (SRS) of 3 or greater based on a 17-segment model. Patients with a typical bundle (n = 26), paced rhythm (n = 2), and Q waves (n = 64) were excluded. Of the remaining 409 patients (mean age, 58 +/- 13 years; 52% male), 155 (38%) had FQRS on the ECG. FQRS patients had a higher mean SSS, SRS, and global summed difference score and a lower left ventricular ejection fraction (all P < .001), as well as greater regional stress MPI scar (69% vs 11%, P < .001). FQRS pattern sensitivity was 75% and specificity was 94% for a corresponding regional MPI scar. On logistic regression, SSS, SRS, summed difference score, left ventricular ejection fraction, and regional scar were univariate predictors of the FQRS pattern on the ECG (all P < .01), and any regional scar (odds ratio, 32; P < .001) was a multivariate predictor. CONCLUSIONS: FQRS complexes on an ECG are a marker of higher stress MPI perfusion and functional abnormalities. Regional FQRS patterns denote the presence of a greater corresponding focal regional myocardial scar on stress MPI.

Prognostic importance of wall motion abnormalities in patients with ischemic cardiomyopathy and an implantable cardioverter-defibrillator.

Patients with extensive regional wall motion abnormalities are predisposed to development of ventricular tachyarrhythmia. The prognostic effect of this in patients with an implantable cardioverter-defibrillator (ICD) and coronary artery disease (CAD) is not known. Echocardiographic left ventricular systolic indexes, wall motion score index (WMSI), and extent of regional akinesia in 140 patients (65 +/- 10 years old; 92% men) with an ICD and CAD were studied. Arrhythmic events requiring ICD therapy and causing death (n = 41, 29%) were recorded over a mean follow-up of 1.4 +/- 0.8 years. Left ventricular basal fractional shortening, ejection fraction, global WMSI, and extent of akinesia, especially in the inferoposterior regions of a right coronary artery territory, were univariate predictors (all p values <0.05). Global WMSI (hazard ratio 2.18, 95% confidence interval 1.03 to 4.65, p = 0.04) and fractional shortening (hazard ratio 0.93, 95% confidence interval 0.88 to 1.00, p = 0.04) were multivariate predictors. Global WMSI (p = 0.04) and > or =2 right coronary region akinetic segments (p = 0.05) provided incremental risk prediction to left ventricular ejection fraction in a global risk-assessment model (chi-square p = 0.001). Presence of right coronary region akinesia better identified those at increased risk of events (p = 0.02) compared with the presence of left anterior descending region akinesia (p = 0.2), independent of systolic function. In conclusion, global WMSI and left ventricular basal fractional shortening were important additional risk predictors of ICD events in CAD. Global WMSI and right coronary region inferoposterior akinesia provided independent and incremental risk assessment to left ventricular ejection fraction and improved identification of those at increased risk of ICD-related events in patients with ischemic cardiomyopathy.

Significance of a fragmented QRS complex versus a Q wave in patients with coronary artery disease.

BACKGROUND: Q waves on a 12-lead ECG are markers of a prior myocardial infarction (MI). However, they may regress or even disappear over time, and there is no specific ECG sign of a non-Q-wave MI. Fragmented QRS complexes (fQRSs), which include various RSR' patterns, without a typical bundle-branch block are markers of altered ventricular depolarization owing to a prior myocardial scar. We postulated that the presence of an fQRS might improve the ability to detect a prior MI compared with Q waves alone by ECG. METHODS AND RESULTS: A cohort of 479 consecutive patients (mean+/-SD age, 58.2+/-13.2 years; 283 males) who were referred for nuclear stress tests was studied. The fQRS included various morphologies of the QRS (<120 ms), which included an additional R wave (R') or notching in the nadir of the S wave, or >1 R' (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory. The Q wave was present in 71 (14.8%) patients, an fQRS was present in 191 (34.9%) patients, and an fQRS and/or a Q wave was present in 203 (42.3%) patients. Sensitivity, specificity, and the negative predictive value for myocardial scar as detected by single photon emission computed tomography analysis were 36.3%, 99.2%, and 70.8%, respectively, for the Q wave alone; 85.6%, 89%, and 92.7%, respectively, for the fQRS; and 91.4%, 89%, and 94.2%, respectively, for the Q wave and/or fQRS. CONCLUSIONS: The fQRS on a 12-lead ECG is a marker of a prior MI, defined by regional perfusion abnormalities, which has a substantially higher sensitivity and negative predictive value compared with the Q wave.

Comparison of diastolic septal perforator flow velocities in hypertrophic cardiomyopathy versus hypertensive left ventricular hypertrophy.

In this study, we measured diastolic septal perforator flow velocities by Doppler transthoracic echocardiography (TTE) in patients with hypertrophic cardiomyopathy (HCM). Using color-guided pulsed Doppler TTE, septal perforator flow velocity recordings were attempted in 69 patients and successfully recorded in 47 (68%). First, we compared 14 patients with HCM to 12 controls and to 11 patients with hypertension with left ventricular hypertrophy. Next, in 10 additional patients with HCM, we compared the septal velocities with the epicardial left anterior descending artery (LAD) velocities recorded during the same TTE study. In the patients with HCM, the peak septal diastolic velocities were twice that of the normal controls (88 +/- 40 vs 41 +/- 13 cm/s) and also higher than in hypertensive left ventricular hypertrophy (51 +/- 18 cm/s, p < 0.0001). All 10 patients with HCM showed a step-up of peak diastolic velocity from the LAD to the septal perforator from 41 +/- 9 to 72 +/- 17 cm/s (p < 0.0001). Three patients with HCM had surgical septal myectomy. These patients had luminal narrowings of the small intramural arteries at histopathologic examination. In conclusion, pulsed Doppler measurement of septal perforator flow velocities is feasible. In HCM, the epicardial coronary arteries enlarge to accommodate increased flow, and diastolic velocity is normalized. In contrast, the increased velocities in the septal branches of patients with HCM are similar to those previously observed in tunnel-like obstructions. These findings suggest that in HCM, notwithstanding an increase in coronary flow, hemodynamically significant narrowings are present in the septal branches. Doppler TTE may become useful for evaluation of abnormal intramural coronary flow in HCM.

Comparison of prognostic value of stress echocardiography versus stress electrocardiography in patients with suspected coronary artery disease.

Stress electrocardiographic (ECG) ST-segment depression is a prognostic marker of adverse cardiac outcomes in coronary artery disease. However, use of concurrent stress echocardiography (ECHO) has lead to concordant and discordant findings on stress electrocardiogram during stress studies. The prognostic value of stress ECHO in the setting of these stress ECG findings has not been previously evaluated. Outcomes of 1,268 patients (60 +/- 12 years old, 48% women) who had normal electrocardiograms and underwent stress ECHO were analyzed. ST-segment depression > or =1.5 mm in 2 contiguous leads on stress electrocardiogram and a wall motion score index of >1 on peak stress echocardiogram were considered abnormal. Events of nonfatal myocardial infarction (n = 18) and cardiac death (n = 32) were analyzed during follow-up (2.8 +/- 0.9 years). In 91 patients (7%) who had abnormal findings on stress electrocardiogram, 38 (41%) had an abnormal finding on stress echocardiogram and 4 had cardiac events (0.6% per year), and all who had a normal finding on stress echocardiogram had no events (n = 53, 59%, p = 0.01). Among 46 events (92%) with a normal finding on stress electrocardiogram, 30 (60%) showed a discordantly abnormal finding on stress echocardiogram (3.2% per year, p <0.01). Overall, the cohort that had normal findings on stress echocardiogram showed a lower event rate (72%, 16 events, 1.1% per year) compared with the cohort that had abnormal findings on stress echocardiogram (28%, 34 events, 3.6% per year, p <0.001), independent of stress ECG response. Peak wall motion score index (hazard ratio 2.55, p <0.001) and left ventricular ejection fraction (hazard ratio 0.99, p <0.001) were independent and incremental (global chi-square, p <0.001) prognostic markers by stress ECHO. In conclusion, a normal finding on stress echocardiogram confers a benign prognosis independent of the type of stress ECG response during stress studies. In addition, peak wall motion score index and ejection fraction by ECHO are stronger prognostic markers over stress electrocardiography in patients who are evaluated for coronary artery disease.

Comparison of tissue Doppler dynamics to Doppler flow in evaluating left atrial appendage function by transesophageal echocardiography.

Tissue Doppler imaging (TDI) patterns from the left atrial appendage (LAA) were evaluated by transesophageal echocardiography. Reproducible, characteristic triphasic or biphasic tissue velocities similar to Doppler flow of the LAA were obtained. Patient peak TDI velocities correlated well with flow and were measurable in atrial fibrillation. Patients with an embolic cerebrovascular accident and in sinus rhythm had higher tissue TDI velocities from the LAA compared with patients without an event, and the groups had similar flow velocities. Hence, Doppler tissue contraction dynamics determined by TDI may complement flow velocities in evaluating LAA function for risk assessment of thromboembolism.

Exercise acutely increases circulating endothelial progenitor cells and monocyte-/macrophage-derived angiogenic cells.

OBJECTIVES: We investigated whether a single episode of exercise could acutely increase the numbers of endothelial progenitor cells (EPCs) and cultured/circulating angiogenic cells (CACs) in human subjects. BACKGROUND: Endothelial progenitor cells and CACs can be isolated from peripheral blood and have been shown to participate in vascular repair and angiogenesis. We hypothesized that exercise may acutely increase either circulating EPCs or CACs. METHODS: Volunteer subjects (n = 22) underwent exhaustive dynamic exercise. Blood was drawn before and after exercise, and circulating EPC numbers as well as plasma levels of angiogenic growth factors were assessed. The CACs were obtained by culturing mononuclear cells and the secretion of multiple angiogenic growth factors by CACs was determined. RESULTS: Circulating EPCs (AC133+/VE-Cadherin+ cells) increased nearly four-fold in peripheral blood from 66 +/- 27 cells/ml to 236 +/- 34 cells/ml (p < 0.05). The number of isolated CACs increased 2.5-fold from 8,754 +/- 2,048 cells/ml of peripheral blood to 20,759 +/- 4,676 cells/ml (p < 0.005). Cultured angiogenic cells isolated before and after exercise showed similar secretion patterns of angiogenic growth factors. CONCLUSIONS: Our study demonstrates that exercise can acutely increase EPCs and CACs. Given the ability of these cell populations to promote angiogenesis and vascular regeneration, the exercise-induced cell mobilization may serve as a physiologic repair or compensation mechanism.