In vivo fluid dynamics of the Ventura interatrial shunt device in patients with heart failure.

AIMS: Interatrial shunts are under evaluation as a treatment for heart failure (HF); however, their in vivo flow performance has not been quantitatively studied. We aimed to investigate the fluid dynamics properties of the 0.51 cm orifice diameter Ventura shunt and assess its lumen integrity with serial transesophageal echocardiography (TEE). METHODS AND RESULTS: Computational fluid dynamics (CFD) and bench flow tests were used to establish the flow-pressure relationship of the shunt. Open-label patients from the RELIEVE-HF trial underwent TEE at shunt implant and at 6 and 12 month follow-up. Shunt effective diameter (Deff) was derived from the vena contracta, and flow was determined by the continuity equation. CFD and bench studies independently validated that the shunt's discharge coefficient was 0.88 to 0.89. The device was successfully implanted in all 97 enrolled patients; mean age was 70 ± 11 years, 97% were NYHA class III, and 51% had LVEF ≤40%. Patency was confirmed in all instances, except for one stenotic shunt at 6 months. Deff remained unchanged from baseline at 12 months (0.47 ± 0.01 cm, P = 0.376), as did the trans-shunt mean pressure gradient (5.1 ± 3.9 mmHg, P = 0.316) and flow (1137 ± 463 mL/min, P = 0.384). TEE measured flow versus pressure closely correlated (R2 ≥ 0.98) with a fluid dynamics model. At 12 months, the pulmonary/systemic flow Qp/Qs ratio was 1.22 ± 0.12. CONCLUSIONS: When implanted in patients with advanced HF, this small interatrial shunt demonstrated predictable and durable patency and performance.

Left atrial remodeling postseptal myectomy for severe obstructive hypertrophic cardiomyopathy: Analysis by two-dimensional speckle-tracking echocardiography.

BACKGROUND: Septal myectomy relieves left ventricular outflow obstruction (LVOTO) and is associated with excellent long-term outcomes. LVOTO is associated with diastolic dysfunction and increased left atrial (LA) size. We sought to investigate the changes in LA volumes and function postmyectomy and the association between these changes with clinical outcomes postmyectomy. METHODS: Sixty-six hypertrophic cardiomyopathy patients undergoing myectomy were retrospectively studied. Preprocedural and 6- to 18-month postmyectomy follow-up transthoracic echocardiographic images were obtained. LA volumes and strain were assessed by two-dimensional speckle-tracking echocardiography. RESULTS: Left atrial volumes, that is, indexed maximal, minimal, and pre-A volumes reduced postmyectomy, yet remained increased compared to controls (105.6 ± 34.5 mL vs 84.9 ± 26.7 mL, 45.2 ± 25.7 mL vs 35.4 ± 22.6 mL, 70.1 ± 31.4 mL vs 35.4 ± 22.6 mL, respectively, P < 0.05). The total emptying index did not improve postmyectomy and remained lower than controls (58.6 ± 12.4 vs 59.9 ± 12.8, P = NS) whereas atrial contraction improved, yet did not normalize (active emptying index 36.1 ± 14.9 vs 41.1 ± 16.2, P < 0.05). The conduit volume remained reduced postmyectomy (18.6 ± 13.3 mL vs 16.6 ± 15.1 mL, P = NS). LA strain also did not improve postmyectomy (26.8 ± 7.3 vs 28.5 ± 8.8, P = NS). A multivariable logistic regression identified preprocedural E/e' ratio and indexed maximal LA volume, as independent predictors for LA volume reduction ≥20% postmyectomy. During a mean follow-up of 4.9 ± 2.3 years postmyectomy, 24.2% of the patients developed atrial fibrillation and <5% of patients were severely symptomatic. We found no associations between LA volumes/function and atrial fibrillation or symptoms postmyectomy. CONCLUSION: Postmyectomy LA volumes decreased, and the contractile function improved. There was no association between LA volumes/function and clinical outcomes postmyectomy. Notably, the LA remained enlarged (though to a lesser degree) with reduced strain and emptying fraction, suggesting possible atrial myopathy.

Myocardial fibrosis in hypertrophic cardiomyopathy: accurate reflection of histopathological findings by CMR.

OBJECTIVES: In this study we sought to explore the relationship between cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) and histopathological parameters including interstitial fibrosis and replacement fibrosis (scar) in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: CMR-LGE is a well-established tool for the assessment of scar in ischemic heart disease. Its role in HCM has evolved in recent years, and an association with nonsustained ventricular tachycardia has been demonstrated. METHODS: HCM patients who underwent septal myectomy during the period 2004 through 2010 and had undergone CMR-LGE no more than 6 months before surgery were selected. Histopathological assessment of the myectomy specimens included quantitative digital analysis (interstitial and replacement fibrosis) and semiquantitative assessment (small intramural coronary arteriole dysplasia and disarray). Correlations between CMR-LGE measured with various techniques, SD above the signal intensity for the normal remote myocardium (2, 4, 5, 6, and 10 SD) and the full width at half maximum (FWHM) technique, at the myectomy site, and interstitial fibrosis, replacement fibrosis (scar), and their sum (fibrosis + scar) were evaluated. RESULTS: Twenty-nine patients were included. Statistically significant correlations between CMR-LGE (at 2, 4, 5, 6, 10 SD and by the FWHM technique), and both interstitial fibrosis and the combined interstitial and replacement fibrosis were found. The strongest correlation was between combined interstitial and replacement fibrosis and CMR-LGE measured at 5 SD (r = 0.78, p < 0.0001). LGE measured at 10 SD demonstrated the best correlation with replacement fibrosis (r = 0.42, p = 0.02). Bland-Altman analysis revealed optimum agreement between the combined interstitial and replacement fibrosis found at pathology and LGE measured at 4 SD. In addition, moderate and severe small intramural coronary artery dysplasia showed a statistically significant correlation with replacement fibrosis (p = 0.01) and CMR-LGE at 10 SD (p = 0.04). CONCLUSIONS: CMR-LGE measured at 4 SD and 5 SD yields the closest approximation to the extent of total fibrosis measured by the histopathological standard of reference. These findings have implications for future investigations of CMR-LGE and its association with important clinical endpoints in HCM, including sudden cardiac death.

Can dobutamine stress echocardiography induce cardiac troponin elevation?

BACKGROUND: Elevation of cardiac troponin (cTn) is considered specific for myocardial damage. Elevated cTn and echocardiogrpahic documentation of wall motion abnormalities (WMAs) that were recorded after extreme physical effort raise the question whether dobutamine stress echo (DSE), can also induce elevation of troponin. METHODS: we prospective enrolled stable patients (age >18 years) referred to DSE. The exam was performed under standardized conditions. Blood samples for cTnI were obtained at baseline and 18-24 hours after the test. We aimed to compare between the clinical and echocardiographic features of patients with elevated cTnI and those without cTnI elevations. RESULTS: Fifty-seven consecutive patients were included. The average age was 64.4 ± 10.7, 73% of the patients were males, and nearly half of the patients were known to have ischemic heart disease. Two of the patients were excluded due to technical difficulty. No signs of ischemia were recorded in 25 (45.4%). Among the patients with established ischemia on DSE, 12 (22%) had mild ischemia, 13 (23.6%) had moderate and 5 (9%) had severe ischemia. Angiography was performed in 13 (26%) of the patients, of which 7 had PCI and one was referred to bypass surgery. None of the patients had elevated cTnI 18-24 hours after the DSE. CONCLUSIONS: Our results indicate that there is no elevation of cTn despite the occurrence of significant WMAs on DSE. We conclude that cTnI cannot be used as an additional diagnostic tool during pharmacological stress test performed to evaluate the presence and severity of ischemia.

Intracoronary administration of autologous bone marrow mononuclear cells in patients with chronic ischemic symptomatic cardiomyopathy: 5 years follow-up.

BACKGROUND: Several studies have demonstrated the shortterm safety, feasibility and efficacy of cell transplantation in patients with advanced heart failure. Data on the long-term outcome are lacking. OBJECTIVES: To evaluate the long-term outcome of intracoronary autologous bone marrow administration in patients with stable severe ischemic cardiomyopathy who were not suitable for revascularization. METHODS: We enrolled eight consecutive patients with ischemic cardiomyopathy: all were in NYHA functional class III-IV despite optimal medical treatment. Dobutamine stress echo showed that all had left ventricular ejection fraction < 35% with significant viability or ischemia, or both, in at least two myocardial segments. Based on coronary anatomy none of the patients was suitable for revascularization. Bone marrow was obtained and the cells were injected into all patent conduits after a brief balloon occlusion at a normal coronary segment. Clinical followup was performed periodically at the heart failure clinic, and included electrocardiography, laboratory tests and echocardiography. RESULTS: During 5 years follow-up there were two deaths: one due to leukocytoclastic vasculitis 21 months after intracoronary bone marrow infusion, and the second patient died suddenly during sleep 30 months after the transplant. The other six patients are alive, two of them without any cardiovascular or clinical events. No significant change in systolic and diastolic function was observed on echocardiography. CONCLUSIONS: Despite the small and selected patient group, our long-term follow-up showed a promising outcome for this population of patients suffering from severe cardiac disease. Longer follow-up of a much larger group is needed.

Acute myocardial infarction with spontaneous reperfusion: clinical characteristics and optimal timing for revascularization.

BACKGROUND: Spontaneous coronary reperfusion occurs in 7-27% of patients with ST elevation myocardial infarction, and is an independent predictor of myocardial salvage, percutaneous coronary intervention success, and improved outcome. OBJECTIVES: To determine the optimal PCI time for patients admitted to the hospital due to STEMI with SCR. METHODS: We performed a retrospective analysis of all patients admitted to the coronary care unit between July 2002 and November 2004 with a diagnosis of STEMI with SCR. RESULTS: The study group comprised 86 patients. There was not a single reinfarction episode during an observation period of 6579 patient hours. Cardiac catheterization was executed early (< 24 hours from pain onset) in 26 patients and late (> 24 hours) in 55. Pre-PCI angiographic TIMI flow 2-3 was seen in > 95% in both groups. PCI was performed more frequently in the "early" group (P = 0.024), while multi-vessel coronary artery disease (P = 0.094) requiring coronary bypass surgery (P = 0.056) was observed more frequently in the "late catheterization" group. Myocardial infarction and angina pectoris at 30 days occurred more frequently in the early catheterization group (P = 0.039), however no difference in any major adverse cardiac events was detected during long-term follow-up (491 +/- 245 days). CONCLUSIONS: Reinfarction after STEMI with SCR is a rare event. Early PCI in patients with STEMI and SCR, even when executed with aggressive antiplatelet therapy, seems to result in an excess of early MACE without any long-term advantage. Prospective randomized trials should determine the optimal PCI timing for these patients.