Cardiac Valve Injury Research Articles

Traumatic Papillary Muscle Rupture Mimicking Infective Endocarditis

Blunt trauma due to motor vehicle accident may result in severe cardiac valve injury. The most part of lesions are about aortic and mitral valves. Acute on-set cardiac valve insufficiency may cause severe dyspnea or cardiac failure. Tricuspid valve injury due to blunt trauma is extremely rare and clinical manifestation is silent in majority of all cases. In case of echocardiographic evaluation, patient can be diagnosed easily with cardiac valve injury. Here we introduce a 46 year-old male patient suffering tricupid papillary muscle rupture and its successful surgical repair. Fever and a mass on the valve caused by multitrauma may mimic infective endocarditis.

Cholesterol crystal induced inflammation and mechanical cardiac valve injury: Implications for transcatheter aortic-valve replacement

The process of cardiac valve sclerosis and stenosis in non-rheumatic disease is related to inflammation via the innate immune system similar to atherosclerosis. Cardiac valve composition shares many features with arterial tissue. Cholesterol infiltration in the valve matrix results in cholesterol crystal formation and deposition that causes mechanical injury and triggers inflammation. Sclerotic human valve specimens as well as valves from atherosclerotic rabbit models reveal presence of cholesterol crystals and macrophage infiltration as seen in atherosclerosis. Lipid lowering by combination of simvastatin and ezetimibe demonstrates cholesterol reduction in valves only if used in a preventive manner. However, once the valve is infiltrated by cholesterol and crystals form in the tissue matrix, these become very difficult to extract and lipid lowering is no longer very effective. Furthermore, cholesterol crystals serve as a nidus for calcium phosphate deposition that distorts and stiffens the valve tissue leading to valve dysfunction. During Transcatheter Aortic Valve Replacement (TAVR) procedures, crystals can complicate the procedure by release of crystalline particles causing ischemic cerebral events and rupturing balloons.

0235: Contribution of endothelial cells, serotonergic 5-HT2A and 5-HT2B receptors and eNOS in early processes of valve degeneration due to nordexfenfluramine in mice

Chronic use of 5-HT 2B receptor (5-HT 2B -R) agonists (anorectic drugs or ergot derivatives) has been associated with left cardiac valve injury but the mechanisms are unclear. Lesions are characterised by increased thickness and cellularity with massive extracellular matrix production. This work was designed to study contribution of 5-HT 2B and 5-HT 2A -R and the link with their activation and endothelial nitric oxide in valve degeneration. We validated an experimental mouse model of valvulopathy by infusing (28 days; Alzet ® pumps) the selective 5-HT 2B -R agonist (nordexfenfluramine: NdF 1 mg/kg/day) and designed 13 groups: 5 groups of WT mice (129svPas; 12 weeks): 1) control (C); 2) NdF; 3) NdF+ritanserine (2 mg/kg/day); 4) NdF+SB206553 (1 mg/kg/day); 5) NdF+LNAME (300 mg/kg/day); 8 groups of transgenics: 6) 5-HT 2B -/- -C; 7) 5-HT 2B -/- - NdF; 8) 5-HT 2A/2B -/- -C; 9) 5-HT 2A/2B -/- -NdF; 10) 5-HT 2A -/- -C and 11) 5-HT 2A -/- - NdF and 2 groups of eNOS -/- mice 12) eNOS -/- -C and 13) eNOS -/- -NdF. Mice were monitored for hemodynamic and echocardiographic parameters. At day 28, blood 5-HT and urinary 5-HIAA concentrations were measured and hearts harvested for histological analysis. In controls, this analysis reveals mitral valve lesions with increased thickness (WT-C 35±4μm vs WT-NdF 69±9μm; p<0,05) and number of endothelial cells (+40%). Lesions are fully prevented by pharmacological and constitutive inactivation of: 5-HT 2B -R (SB 206553 or 5-HT 2B -/- mice) and both 5-HT 2A and 5-HT 2B -R (ritanserine or 5-HT 2A/2B -/- ). In 5-HT 2A -/- treated with NdF, we still observe an increased valve thickness (5-HT 2A -/- -C 45±4μm vs 5-HT 2A -/- -NdF 60±8μm) mainly due to increased cellularity. Finally, eNOS inhibition (L-NAME or eNOS -/- mice) also prevents lesions indicating the crucial role of endothelial cells in 5-HT 2B -mediated mitral valve degeneration. We demonstrate for the first time that both 5-HT 2B and 5-HT 2A -Rs are involved in drug-induced valvulopathy and the role of endothelial cells and eNOS activation.

Traumatic mitral valve and pericardial injury.

Cardiac injury after blunt trauma is common but underreported. Common cardiac trauma after the blunt chest injury (BCI) is cardiac contusion; it is very rare to have cardiac valve injury. The mitral valve injury during chest trauma occurs when extreme pressure is applied at early systole during the isovolumic contraction between the closure of the mitral valve and the opening of the aortic valve. Traumatic mitral valve injury can involve valve leaflet, chordae tendineae, or papillary muscles. For the diagnosis of mitral valve injury, a high index of suspicion is required, as in polytrauma patients, other obvious severe injuries will divert the attention of the treating physician. Clinical picture of patients with mitral valve injury may vary from none to cardiogenic shock. The echocardiogram is the main diagnostic modality of mitral valve injuries. Patient's clinical condition will dictate the timing and type of surgery or medical therapy. We report a case of mitral valve and pericardial injury in a polytrauma patient, successfully treated in our intensive care unit.

Benfluorex‐induced cardiac valve injury

Benfluorex‐induced cardiac valve injury

Tricuspid valve chordal rupture due to airbag injury and review of pathophysiological mechanisms

Blunt trauma to the chest is associated with significant morbidity and mortality. The latter is usually due to an aortic transection, whereas the former is related to myocardial contusion, cardiac valve injury, coronary artery disruption and intracardiac shunts due to the formation of septal defects. The main mechanisms causing these injuries are due to the sudden deceleration force and compression within the chest cavity. Moreover, there is also the sudden increase in intravascular pressure due to a mechanical compression effect and a hormonal adrenergic surge during the event. We report a case of a tricuspid valve injury caused by the deployment of the airbag during a high-speed impact car accident and the subsequent damage to the tricuspid valve chordal mechanism. The patient's management and the pathophysiological mechanisms involved in the injury are reviewed.

Abstract P201: Patient Demographics, Complications, and Hospital Utilization of Pacemaker Implantation in the Extreme Elderly

Introduction: There are scant data for pacemaker implant complications and readmission rates in the extreme elderly (age≥80 years) despite their common use in this population. Methods: This is a retrospective chart review of 149 consecutive patients (age≥80 years) who underwent pacemaker implantation at a community hospital Electrophysiology program from July 2008 through June 2010. Single-, dual-, and biventricular-chamber pacemakers and generator changes were included for analysis; cardioverter-defibrillator devices, temporary pacemakers, and loop recorders were excluded. Standard procedures for implantation were used. Major complications defined as death, cardiac arrest, cardiac perforation, cardiac valve injury, coronary venous dissection, hemothorax, pneumothorax, transient ischemic attack, stroke, myocardial infarction, pericardial tamponade, and arterial-venous fistula. Minor complications defined as drug reaction, conduction block, hematoma or lead dislodgement requiring reoperation, peripheral embolus, phlebitis, peripheral nerve injury, and device-related infection. Results: The baseline demographics, complication rates, and hospital utilization are shown in the Table below. There were no intraprocedural complications. There was one major in-hospital (0.7%) and one minor in-hospital complication (0.7%). Within 30 days of implant, there were 2 minor (1.3%) and 4 major (2.7%) complications. Eight of 149 patients (5.4%) were readmitted within 30days of implantation. Conclusions: This report of pacemaker implantations in the extreme elderly reveals rates of complications comparable to data from younger patient populations.

Pacemaker implantation in the extreme elderly

There are scant data for pacemaker implant complications and readmission rates in the extreme elderly (age ≥80 years) despite their common use in this population. This is a retrospective chart review of consecutive patients (n = 149, age ≥80 years) who underwent pacemaker implantation at a community hospital electrophysiology program from July 2008 through June 2010. Single-, dual-, and biventricular-chamber pacemakers and generator changes were included for analysis; cardioverter-defibrillator devices, temporary pacemakers, and loop recorders were excluded. Standard procedures for implantation were used. Major complications were defined as death, cardiac arrest, cardiac perforation, cardiac valve injury, coronary venous dissection, hemothorax, pneumothorax, transient ischemic attack, stroke, myocardial infarction, pericardial tamponade, and arteriovenous fistula. Minor complications were defined as drug reaction, conduction block, hematoma or lead dislodgement requiring reoperation, peripheral embolus, phlebitis, peripheral nerve injury, and device-related infection. The overall mean age of implantation was 86 years. There were no intraprocedural complications. There was one major in-hospital complication (0.7%) and one minor in-hospital complication (0.7%). Within 30 days of implantation, there was an overall 5.4% rate of complications; four minor (2.7%) and four major (2.7%). There was a 30-day cardiovascular-attributable mortality of 0.7% and an all-cause mortality of 2%. There was a 5.4% rate of readmission within 30 days of implantation. This report of pacemaker implantations in the extreme elderly reveals rates of implant complications comparable to data from younger patient populations while experiencing a higher 30-day all-cause mortality (that may be attributable to elevated all-cause mortality rates in this age group).

Acute Aortic Valve Rupture Secondary to Blunt Chest Trauma

Cardiac valve injury after blunt chest trauma is rare. We present a case of blunt chest trauma resulting in an isolated aortic valve rupture treated with aortic valve replacement.

Cardiac Valvular Pathology: Comparative Pathology and Animal Models of Acquired Cardiac Valvular Diseases

Recent voluntary withdrawal of the ergoline-derivative Alzheimers' drug Pergolide (Permax) resulting from demonstrated risk of cardiac valve injury illustrates the increased importance of valve injury in pharmaceutical toxicology. Following the 2001 landmark discovery of cardiac valve injury associated with the widely prescribed anti-obesity drug combination fenfluramine-phentermine, and subsequent withdrawal, the need to understand and assess cardiac valve biology and pathology both preclinically and clinically has been accentuated. Unique aspects of the developmental biology, anatomy, and physiology of cardiac valves compared to main cardiac tissue have been discovered, and key elements of the pathophysiology of various valvular injury mechanisms have been described. Although general clinical cardiac valvular disease in humans has been well characterized, animal modeling of valvular injury has proved to be difficult and undersubscribed. Additionally, both the preclinical, pharmaceutical, toxicologic assessment of valvular injury and the understanding of species-comparative valvular pathology have been limited. As discoveries and awareness grows, the purpose of this paper is to review the structure and function of cardiac valves, mechanisms, and outcomes of the common acquired human cardiac valve diseases, including those that are drug-related; to summarize comparative laboratory animal valvular pathology; and to review the literature of contemporary animal models of valvular injury.

ENDOTHELIUM-DERIVED MICROPARTICLES INHIBIT HUMAN CARDIAC VALVE ENDOTHELIAL CELL FUNCTION

Elevated numbers of endothelium-derived microparticles (EMPs) in the circulation are found in a variety of critical illnesses. EMPs have been associated with vascular dysfunction, including thrombotic complications and loss of normal vascular reactivity, common responses associated with cardiac valve injury. However, the exact mechanisms of this dysfunction and the potential impact on cardiac endothelium are unknown. We hypothesize that pathologic levels of circulating EMPs negatively regulate proliferation and migration of valvular endothelial cells (ECs), leading to downstream endothelial dysfunction. EMPs were generated from plasminogen activation inhibitor 1-stimulated human umbilical vein endothelial cells (HUVECs). Human mitral valve endothelial cells (HMVECs) were isolated and characterized by platelet endothelial cell-derived adhesion molecule-1 (PECAM-1, or CD31) and von Willebrand factor immunocytochemistry. HMVECs were treated with increasing EMP doses, and then, the effects of EMPs on growth factor-induced proliferation and migration were tested. Proliferation was assessed by H-thymidine incorporation. EC migration was assayed by photographing microtubules of HMVECs and HUVECs in fibrin gel incubated with EMPs +/- growth factors for 48 h. The EMP effects on non-valve HUVECs were tested in parallel. EMPs inhibited HMVEC proliferation at high doses but stimulated HUVEC proliferation at all doses. In HMVECs, EMPs inhibited basic fibroblast growth factor- and vascular endothelial growth factor-induced proliferation and migration. Taken together, these data suggest EMPs regulate valvular EC proliferation in a dose-dependent manner and, furthermore, modulate growth factor signaling in ECs. These results implicate EMPs as a possible source of downstream EC dysfunction in disease states. EMPs may play a role in valvular leaflet injury in human disease by inhibiting normal growth and repair of endothelium.

Cardiac valve injury with major chest trauma.

The diagnosis of cardiac valve injury with major chest trauma is often delayed. An experience with four patients illustrates the clinical syndromes that may occur. Nonpenetrating blunt chest trauma produced the valve injury in three patients, and the fourth received a shotgun wound. Injury to the tricuspid valve was masked by the associated thoracic trauma in both patients with this lesion, but progressive deterioration led to successful valve replacement ten years and five months after injury. Rupture of the mitral valve produced progressive respiratory failure that was reversed by emergency valve replacement in the third patient. The fourth patient has remained stable without operative treatment for acute aortic insufficiency resulting from the shotgun pellets. At present, serial electrocardiography is the best diagnostic method for early detection of cardiac injury with nonpenetrating chest trauma.