Disease relevance of Tricuspid Valve Insufficiency

• CONCLUSION: Noninvasive assessment of pulmonary hypertension using continuous-wave Doppler of tricuspid regurgitation can predict morbidity and mortality in patients with ischemic or idiopathic dilated cardiomyopathy [1].
• Three patients had congestive cardiomyopathy, two with tricuspid regurgitation; of the remaining three, one had cor pulmonale complicated by tricuspid regurgitation, one had thrombophlebitis and one had no discernible cardiac illness [2].
• An abnormal Doppler echocardiogram of the inferior vena cava (tricuspid regurgitation or impaired right ventricular compliance, or both) predicted the presence of pulmonary arterial hypertension with a sensitivity of 87% and a specificity of 80% [3].
• Echo Doppler measurements of pulmonary blood flow acceleration time (AT) and ejection time (ET), and of the peak velocity of the tricuspid regurgitation jet (TR), were obtained under normobaric conditions of normoxia (fraction of inspired oxygen, FIO2, 0.21), of hyperoxia (FIO2 1.0), and of hypoxia (FIO2 0.125) [4].
• RESULTS: In patients with RA, the prevalence of aortic regurgitation (17%) and tricuspid regurgitation (17%) was not higher than that seen in controls (15% and 6%) [5].

High impact information on Tricuspid Valve Insufficiency

• Massive dilation of the inferior vena cava. Association with tricuspid regurgitation [6].
• Severe, chronic pulmonary arterial banding for 14 days resulted in right ventricular dilatation and dysfunction, associated with right atrial enlargement, and angiographic evidence of tricuspid regurgitation [7].
• Increased right ventricular afterload mediated by constriction of the pulmonary artery and infusion of methoxamine reversibly converted the right atrial pressure-volume loop from that of mild to that of severe tricuspid regurgitation [8].
• Infusion of dobutamine increased the size of the a-loop relative to the v-loop both at baseline and after induction of tricuspid regurgitation [8].
• BACKGROUND: Severe tricuspid regurgitation caused by a PPM or ICD lead is an under-recognized but treatable etiology of severe right heart failure [9].

Chemical compound and disease context of Tricuspid Valve Insufficiency

• It was concluded that amlodipine has the potential to block hypoxic pulmonary vasoconstriction as evidenced by a drug concentration-related decrease in resting tricuspid regurgitation jet velocity without any change in resting myocardial contractility [10].
• However, CAVT reduced the incidence of tricuspid regurgitation and attenuated the elevation in resting ANP secretion [11].
• In the subgroup treated by digoxin as first-line therapy (n = 32), the interval to sinus rhythm restoration was also significantly higher in the presence of tricuspid regurgitation, with a slightly but not significantly lower reduction rate [12].
• In the presence of significant tricuspid regurgitation, steroid-eluting active-fixation leads should be used routinely, and in patients with a tricuspid prosthesis, the use of a dedicated cardiac venous pacing system is likely to be the best option [13].
• After injection of hand-agitated 5% glucose and sonicated albumin, trivial tricuspid regurgitation signals were enhanced in 25 of 28 patients (89%) [14].

Biological context of Tricuspid Valve Insufficiency

• In addition, the inferior vena cava was dilated and during contrast echocardiography, contrast echoes appeared during systole suggesting tricuspid regurgitation [15].
• CONCLUSIONS: There is no relationship between tricuspid regurgitation and the levels of maternal serum free beta-hCG and PAPP-A in cases with trisomy 21 [16].

Anatomical context of Tricuspid Valve Insufficiency

• A patient with tricuspid regurgitation by clinical evaluation, cardiac catheterization, and angiography was found at autopsy to have a cardiomyopathy involving both ventricles but with predominant involvement of the right ventricle [17].
• CONCLUSIONS: Damage to the tricuspid valve by PPM or ICD leads may result in severe symptomatic tricuspid regurgitation and may not be overtly visualized by echocardiography [9].
• Multivariate logistic regression models showed that high injection rate, tricuspid regurgitation, pulmonary hypertension, and right ventricular systolic dysfunction were independent predictors of retrograde inferior vena cava or hepatic vein opacification (p < 0.05 for each) [18].
• We performed a successful Batista operation with aortic valve replacement (AVR), graft replacement of the ascending aorta, and tricuspid annuloplasty for a patient with valvular cardiomyopathy with severe aortic stenosis, an ascending aortic aneurysm, and grade 3 tricuspid regurgitation [19].

Gene context of Tricuspid Valve Insufficiency

• The elevation in absolute and fractional CK-MB 42.0 U.l-1 (5.1%) in respect of the infants with TTI (transient tricuspid incompetence) was significant (P less than 0.05) when compared with the controls with features of TTN (transient tachypnoea of the newborn) in the 6-8 h post-partum period [20].
• Pulsatile varicose veins associated with tricuspid regurgitation [21].
• Tricuspid regurgitation with postinfarction ventricular septal defect [22].
• The purpose of this study was to assess the factors involved in the development of the right-to-left (R-L) shunt in patients with atrial septal defect (ASD), especially the role of tricuspid regurgitation (TR) [23].
• Preoperatively, all infants had severe tricuspid regurgitation, Great Ormond Street Ebstein echocardiogram scores greater than 1.3:1 (grade 3 or 4) and cardiothoracic ratio greater than 0.85 [24].

Analytical, diagnostic and therapeutic context of Tricuspid Valve Insufficiency

• Pulsed Doppler echocardiography of the inferior vena cava gave normal results in 10 patients and disclosed tricuspid regurgitation in seven patients, impaired right ventricular compliance in seven patients, and both of these abnormalities in one patient [3].
• Presence or absence of tricuspid regurgitation (TR) was determined by Doppler echocardiography in 73 consecutive COPD patients attending a hospital outpatient clinic [25].
• Eighteen patients had no caval or pulmonary venous obstruction or tricuspid regurgitation at catheterization; 2 had isolated superior vena caval obstruction, 3 had isolated pulmonary venous obstruction, 4 patients had severe tricuspid regurgitation, and 1 had a large residual ventricular septal defect [26].
• Usefulness of echocardiographic determined tricuspid regurgitation in predicting event-free survival in severe heart failure secondary to idiopathic-dilated cardiomyopathy or to ischemic cardiomyopathy [27].
• Functional results and data concerning the incidence and severity of graft atherosclerosis (GASC) and tricuspid incompetence (TI) in the intermediate term after orthotopic heart transplantation (HTX) are still striking [28].

References