Transcatheter aortic valve implantation: restoring the qualities of life in old age.

Transcatheter aortic valve implantation (TAVI) is a tremendous therapeutic advance for patients with severe aortic stenosis and high-surgical risk. Since TAVI-treated patients are elderly with multiple co-existing conditions, limited life expectancy and disproportionate health-care expenditures, the aspect of the health-related quality of life (HRQoL) benefits becomes of fundamental importance. Based on recent evidence, TAVI appears to improve significantly HRQoL measures compared with optimal standard care, which are restored to age-adjusted population norms over time.

Anomalous origin of coronary arteries: when one sinus fits all.

A right coronary artery origin from the left coronary sinus and a left coronary origin from the right sinus although rarely encountered during routine cardiac catheterization, they represent two relatively common autopsy findings in young patients suffering sudden cardiac death. The interarterial course of the aberrant artery, between the aortic root and the pulmonary artery has been considered as a malignant variant, because of the higher risk of myocardial ischemia and sudden death. We present two rare cases of ectopic coronary origin from the opposite sinus of Valsalva.

Long-term quality of life improvement after transcatheter aortic valve implantation.

BACKGROUND: Transcatheter aortic valve implantation (TAVI) is a novel therapeutic option for severe aortic stenosis in old patients with high surgical risk. The aim of this study was to assess changes in quality of life (QoL) along with functional status and late survival after this procedure. METHODS: Thirty-six consecutive patients (80.5 ± 5.9 years, 21 men and 15 women) with a logistic Euroscore of 29.7 ± 13.7 underwent TAVI using the 18-Fr CoreValve prosthesis. Aortic valve prosthesis was inserted retrograde using a femoral or a subclavian arterial approach. QoL was evaluated by administering the Short Form 36 (SF-36) tool and the shorter SF-12 version 2 (SF-12v2) questionnaires before and 1-year after TAVI. RESULTS: TAVI was successfully performed in all patients. The estimated 1-year overall survival rate using Kaplan-Meier method was 68%. One-year follow-up also showed a marked improvement in echocardiographic parameters (peak gradient 76.2 ± 26.1 vs 15.4 ± 7.8 mm Hg, P < .001; aortic valve area 0.7 ± 0.1 vs 2.6 ± 2.7 cm(2), P < .001) with a significant change in New York Heart Association class (3 ± 0.7 vs 1.2 ± 0.4, P < .001). Both preprocedural summary SF-36 and SF-12v12 physical and mental scores showed a significant improvement 1 year after TAVI (21.6 vs 46.7, P < .001; 42.9 vs 55.2, P < .001; 22 vs 48.9, P < .001; 43.3 vs 52.2, P < .001, respectively). CONCLUSIONS: Our results show a marked 1-year clinical benefit in functional status and physical and mental health in patients who underwent TAVI.

Cytokine gene polymorphisms are associated with markers of disease severity and prognosis in patients with idiopathic dilated cardiomyopathy.

AIMS: To identify potential genetic associations of five cytokine gene polymorphisms with disease severity and prognosis in patients with idiopathic dilated cardiomyopathy (DCM). METHODS AND RESULTS: Eighty patients with DCM were genotyped for transforming growth factor beta1 (TGF-ß1)+869 T/C (codon10 Leu→Pro), TGF-ß1 +915 G/C (codon25 Arg→Pro), interleukin (IL)-6 -174G/C, tumor necrosis factor-alpha (TNF-α) -308A/G, interferon-gamma (IFN-γ) +874T/A, IL-10 -1082A/G, IL-10 -819T/C and IL-10 -592A/C gene polymorphisms. In homozygous TT patients for TGF-ß1 +869 T/C polymorphism mean VO(2) max was significantly higher than in CC homozygous patients (25.67±6.73ml/kg/min vs. 20.29±6.35 ml/kg/min, p = 0.046), which remained significant only for patients younger than 39 years old after adjusting for age and sex (p = 0.009). C carriers of TGF-ß1 +915 G/C polymorphism are 4.2 times more likely to be in a worse NYHA stage (III-IV) than non C carriers [OR: 4.25, 95% CI (1.53-11.80), p = 0.006]. Patients GG homozygous for IL-6 -174G/C polymorphism presented greater left ventricle end-systolic (p = 0.018) and end-diastolic (p = 0.04) diameters in comparison to the CC homozygous. The AA homozygote for IFN-γ +874T/A polymorphism (p = 0.02) and the combination of the TGF-ß1 +869 T/C and TGF-ß1 +915 G/C genotypes were associated with adverse outcome (p = 0.014). CONCLUSION: Specific cytokine gene polymorphisms seem to be associated with worse prognosis as well as with measures of disease severity in DCM.

Short and long term anti-inflammatory effects of bosentan therapy in patients with pulmonary arterial hypertension: relation to clinical and hemodynamic responses.

OBJECTIVE: We sought to investigate the short- and long- term effects of bosentan therapy on endothelial, inflammatory and fibrotic markers in patients with pulmonary arterial hypertension (PAH) and the relation to clinical and hemodynamic responses. METHODS: We studied 16 patients with moderate-severe idiopathic PAH, in WHO functional class II-IV, despite conventional treatment. Patients received additional treatment with bosentan, 62.5 mg twice daily for 1 month, followed by 125 mg twice daily for 11 months. Study endpoints included 6-min walking distance (6MWD), mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR) and plasma levels of intracellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), IL-6 and brain natriuretic peptide (BNP). Patients were assessed at baseline, 2 months and 12 months after initiation of bosentan. RESULTS: At 2 months there was an improvement in 6MWD (p < 0.001) and functional class (p < 0.001) and a marked fall in PVR (p < 0.001), ICAM-1 (p < 0.001), IL-6 (p < 0.001)and BNP (p = 0.001). At 12 months, 6MWD was further improved (p < 0.001), PVR remained significantly improved (p < 0.001), mPAP was significantly decreased (p < 0.001) and ICAM-1, IL-6 and BNP remained significantly lower (p < 0.001). Significant correlations were found between changes in ICAM-1 and cardiac index (r = 0.59, p = 0.01), IL-6 and PVR (r = 0.51, p = 0.04), BNP and 6MWD (r = -0.53, p = 0.03) and BNP and PAP (r = 0.51, p = 0.04) between 2- and 12-months treatment. CONCLUSIONS: In patients with moderate-severe PAH, the addition of bosentan to therapy, exerts favorable anti-inflammatory effects, which are associated with clinical and hemodynamic improvement.

Percutaneous aortic valve implantation of the Medtronic CoreValve self-expanding valve prosthesis via left subclavian artery access: the first case report in Greece.

This case report describes a percutaneous aortic valve implantation with the Medtronic CoreValve selfexpanding valve prosthesis in a patient with severe aortic stenosis. The approach was made via the left subclavian artery because of the lack of femoral vessel access. The patient was a 78-year-old female with breathlessness on minimal effort, a recent hospitalisation due to pulmonary oedema, and frequent episodes of pre-syncope; surgical valve replacement had been ruled out. The prosthetic valve was successfully implanted with mild paravalvular aortic regurgitation. At 30 days, the patient's clinical condition had significantly improved, with excellent functioning of the aortic valve prosthesis.

Ischaemia-modified albumin in pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) may be associated with subendocardial ischaemia. We investigated whether ischaemia-modified albumin (IMA), an established marker of ischaemia, is elevated in stable patients with PH. METHODS: We studied 32 patients with PH and an equal number of age-matched normal volunteers. We assessed serum IMA levels with the albumin cobalt-binding test. RESULTS: Patients' mean +/- SD (range) pulmonary arterial pressure was 56 +/- 12 (33-73) mmHg and their exercise capacity was 394 +/- 145 (121-688) m in the 6-min walk test. IMA was 92 +/- 14 (69-115) U ml(-1) in the patient group and 93 +/- 9.4 (76-122) U ml(-1) in the control group with no significant difference between the two (p = 0.85), although almost one-third of the patients had detectable troponin-I. CONCLUSIONS: We conclude that IMA, a marker of ischaemia, does not differ in patients with advanced clinically stable PH compared with normal subjects.

Primary stenting of an unprotected left main coronary artery total occlusion in a patient with acute myocardial infraction and cardiogenic shock.

Acute total occlusion of the left main coronary artery (LMCA) is a rare angiographic finding with very poor prognosis. We report a case of a 39-year-old man who presented with pulmonary edema and cardiogenic shock due to an acute anterior myocardial infarction. Coronary angiography, which was performed under the support of an intra-aortic balloon pump, revealed total occlusion of the LMCA. Prompt and successful percutaneous transluminal coronary angioplasty with sirolimus-stent deployment in the LMCA allowed for an uneventful recovery and discharge of the patient.

Repeated exercise stress testing identifies early and late preconditioning.

BACKGROUND: The warm-up phenomenon has been considered to trigger preconditioning. We investigated whether repeated exercise treadmill tests in humans are capable of inducing adaptation to ischemia by triggering both the early and late phase of preconditioning. METHODS: In 25 consecutive patients with stable coronary artery disease, four repeated treadmill tests were performed. Thirty minutes following the first test (T1) a second one was performed (T2), followed 6 h later by a third test (T3). Twenty-four hours later all patients were subjected to a fourth exercise test (T4). In every fifth patient, simultaneous echocardiographic examination was performed at the time of the exercise tests in an attempt to reveal ischemic abnormalities. RESULTS: At baseline there was no difference between the variables. At ST segment depression >1.5 mm, the rate-pressure product (RPP) was higher in T2 and T4 (231.3+/-17.9 and 232.6+/-15.8 mm Hg s 10(2)) than in T1 and T3 (210+/-17 and 210.2+/-16.7 mm Hg s 10(2)), p<0.001. Additionally, time to the onset of chest pain was longer in T2 and T4 (430.8+/-60.5 and 438+/-47 s) than in T1 and T3 (345.6+/-69 and 345.6+/-58 s), p<0.001. At peak exercise, the RPP was higher in T2 and T4 (278.6+/-21.6 and 278.3+/-19.6 mm Hg s 10(2)) than in T1 and T3 (255.6+/-23.1 and 256.6+/-23 mm Hg s 10(2)), p<0.001. The wall motion score index was higher in T1 and T3 (1.65+/-0.17 and 1.53+/-0.16) than in T2 and T4 (1.3+/-0.07 and 1.37+/-0.1), p<0.001. CONCLUSION: By using repeated exercise treadmill tests both the early and late phase of protection can be obtained.

Doppler-derived left ventricular end-diastolic pressure prediction model using the combined analysis of mitral and pulmonary A waves in patients with coronary artery disease and preserved left ventricular systolic function.

The aim of this study was to analyze the components of mitral and pulmonary A waves and to construct a Doppler-derived left ventricular (LV) end-diastolic pressure (EDP) prediction model based on the combined analysis of transmitral and pulmonary venous flow velocity curves. Combined analysis of transmitral and pulmonary venous flow velocity curves at atrial contraction is a reliable predictor of increased LV filling pressure. The duration of pulmonary and mitral A waves is determined by the sum of respective acceleration and deceleration time. Mitral flow and left upper pulmonary vein flow velocity curves were recorded simultaneously with LVEDP in 40 consecutive patients (aged 59 +/- 8 years) with coronary artery disease and preserved LV systolic function. Differences in all parameters represent values of pulmonary minus those of mitral A wave curve. The difference in deceleration time was the strongest candidate, being included in all models. After redundancy evaluation, we reached the following model: LVEDP = 20.61 + 0.229 x difference in deceleration time (r(2) = 0.80, p <0.001). In the entire study group, the difference in duration and in deceleration time of the A wave was highly correlated with LVEDP (r = 0.79, p <0.001, and r = 0.88, p <0.001, respectively). The entire study group was further divided according to whether LVEDP was above (group I, 20 patients) or below (group II, 20 patients) the median value (15.5 mm Hg). In group I, the difference in duration and in deceleration time correlated well (r = 0.62, p = 0.01, and r = 0.75, p = 0.001, respectively) with LVEDP, whereas in group II only the difference in deceleration time correlated well (r = 0.68, p = 0.005). In patients with coronary artery disease and preserved LV systolic function, the combined analysis of mitral and pulmonary A waves can predict LVEDP. The difference in deceleration time between pulmonary and mitral A waves can reliably evaluate high and normal LVEDP.

Angiotensin II fails to induce preconditioning in vivo--the protective role of myocardial stretch due to pressure overload.

BACKGROUND: Angiotensin II (Ang) has been successfully used as a preconditioning analogue in isolated rabbit hearts. It is also known that local concentrations of Ang accelerate ischemic injury in vivo, while activation of stretch receptors protects ischemic hearts. OBJECTIVES: First, to investigate further whether Ang can mimic preconditioning in vivo. Second, to test the hypothesis that there is an activation of stretch receptors, and that the larger infarct from the left atrium Ang compared with that from the intravenous Ang may be associated with the ischemic injury caused by local administration. METHODS: Male rabbits were divided into four groups - a control group, an ischemic preconditioning group with 5 min ischemia, a left atrial group and an intravenous group with 5 min Ang infusion. All animals were subjected to prolonged ischemia and reperfusion. A second series of experiments was also performed with five groups that had a 5 min mechanical obstruction of the aorta (Ao clamp), also used as a preconditioning analogue with or without the stretch receptor blocker gadolinium (Gd). RESULTS: Contrary to what was expected from the ex vivo experiments, Ang failed to mimic preconditioning (infarct size 39.6 6.1%, 13.7 4.1%, 52.2% 6.9% and 31.2 4.8%, respectively for the above groups). Interestingly, however, when Ang was infused intravenously, it produced a significantly smaller infarct compared with that observed after the same dose was infused into the left atrium (P<0.05). The infarct size was 17.0 3.7% in the Ao clamp group, which was an effect completely prevented by Gd (45.8 4.2%, P<0.01). Although Gd did not alter infarct size in the control and ischemic preconditioning groups, it increased infarct size when added to the intravenous Ang group (Gd-intravenous Ang 48.6 3.3%, P<0.05 compared with intravenous Ang). CONCLUSIONS: Ang fails to mimic preconditioning in vivo, but salvage of ischemic myocardium can be emanated from pressure overload.