Transcatheter aortic valve implantation: alternative access options.

Calcific aortic valve stenosis represents the most common acquired valvular heart disease in adults. Transcatheter aortic valve implantation (TAVI) has been established as a widely accepted therapeutic option in elderly and multimorbid patients with severe aortic stenosis not amenable to conventional surgery. Retrograde transfemoral and antegrade transapical approaches are commonly used for implantation. However, there are a certain number of patients who are not candidates for either approach due to poor vascular access, severe pulmonary dysfunction or other prohibitive chest pathologies. Recently, different alternative access route options have been proposed and described. These alternative access routes include approaches via the subclavian/axillary artery, the ascending aorta, the carotid artery, and the brachiocephalic artery.

Simultaneous transcatheter aortic and mitral valve-in-valve implantation in a patient with degenerated bioprostheses and high surgical risk.

Transcatheter valve-in-valve implantation is evolving as a promising alternative to reoperative valve replacement in selected high-risk patients, considering the increasing need for redo surgery due to bioprosthetic degeneration in the future. Reoperative double valve replacements are particularly associated with an elevated surgical risk. The transapical access provides the opportunity to approach the aortic and mitral valves during one intervention. We report the case of a successful transcatheter valve-in-valve implantation in the aortic and mitral position within a single procedure.

Coronary artery anomalies Part II: recent insights from clinical investigations.

Congenital anomalies of the coronary arteries occur in 0.2-1.2% of the general population; they cause 12% of sports-related sudden cardiac deaths and 1.2% of non-sports-related deaths. We review some of the substantial advances that have been made both, in the understanding of the embryonic development of the coronary arteries and in the clinical diagnosis and management of their anomalies. In this second part of our review we elucidate recent approaches to defining coronary anomalies and provide information on their incidence and prognosis. In addition, we discuss the options for screening large populations for potentially lethal coronary malformations and elucidate the role of invasive diagnostic modalities such as intravascular ultrasound, flow wire and pressure wire. The clinical relevance of coronary anomalies is discussed particularly for the ill-defined group of anomalies that only occasionally cause severe clinical events comprising anomalous origination of a coronary artery from the opposite sinus (ACAOS), coronary artery fistulae and myocardial bridging. Finally, we provide an update on current diagnostic and therapeutic recommendations.

Coronary artery anomalies. Part I: Recent insights from molecular embryology.

Congenital anomalies of the coronary arteries occur in 0.2-1.2% of the general population and may cause substantial cardiovascular morbidity and mortality. We review some of the advances that have been made both, in the understanding of the embryonic development of the coronary arteries (part I) and in the clinical diagnosis and management of their anomalies (part II). In this first part of our review we elucidate basic mechanisms of coronary vasculogenesis, angiogenesis and embryonic arteriogenesis. Moreover, we review the role of cellular progenitors such as epicardium-derived cells, cardiac neural crest cells and cells of the peripheral conduction system. Then we discuss the role of growths factors (such as FGV, HIF 1, PDGF B, TGFbeta1, VEGF, and VEGFR-2) and genes (such as FOG-2, VCAM-1, Bves, and RALDH2) at different states of coronary development. and we discuss the role of the cardiac neural crest in the concurrence of coronary anomalies with aortic root malformations. This part of the article is designed to review major determinants of coronary vascular development to provide a better understanding of the multiplicity of options and mechanisms that may give rise to coronary anomaly. To this end, we highlight results from experiments that provide insight in mechanisms of coronary malformation.

[Clinical diagnosis of acute aortic dissection]. / Die klinische Diagnose akuter Aortendissektionen.

Despite the availability of modern imaging technology, 35% of aortic dissections remain undiagnosed in vivo because clinical criteria for aortic dissection are not available to date. The present study analyzed 250 patients with acute chest and/or back pain, absence of an established differential diagnosis of the pain syndrome and clinical suspicion of acute aortic dissection for presence of 26 clinical variables. Multivariate analysis identified an aortic pain syndrome with immediate onset and/or tearing or ripping character (P < 0.0001), mediastinal and/or aortic widening on chest radiography (P < 0.0002) and pulse- and/or blood pressure differentials (P < 0.0001) as predictors of acute aortic dissection. Probability of dissection was low (7%) with absence of all three variables, intermediate (31 and 39%, respectively) with isolated findings of "aortic pain" or "mediastinal widening", and high (> 83%) with either isolated "pulse- and/or blood pressure differentials" or any combination of the three variables. This model appears useful to improve selection of patients for emergency imaging of the thoracic aorta.

Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume and composition in patients with coronary artery disease.

BACKGROUND: We studied whether lipid-lowering therapy with atorvastatin (target LDL cholesterol [LDL-C] <100 mg/dL) compared with a moderate treatment regimen that used other lipid-lowering drugs led to a lesser progression of atherosclerosis and to different changes in plaque echogenicity in patients with coronary artery disease. METHODS AND RESULTS: This study was a 12-month, open-label, randomized, multicenter trial, which used serial 3D intracoronary ultrasound to calculate plaque volume and plaque echogenicity. After transcatheter therapy, 131 patients were randomized (atorvastatin n=65, usual care n=66). The target plaque had to be a minor lesion (ie, a diameter stenosis of <50% on angiography). After 12 months, mean LDL-C was reduced from 155 to 86 mg/dL in the atorvastatin group and from 166 to 140 mg/dL in the usual care group. Mean absolute plaque volume showed a larger increase in the usual care group compared with the atorvastatin group (usual care 9.6+/-28.1 mm(3), atorvastatin 1.2+/-30.4 mm(3); P=0.191). The hyperechogenicity index of the plaque increased to a larger extent for the atorvastatin group than for the usual care group, with a significant treatment effect for the percent change (atorvastatin 42.2%, usual care 10.1%; P=0.021). CONCLUSIONS: One year of lipid-lowering therapy to <100 mg/dL LDL-C most likely led to a slowdown of plaque growth of minor lesions. The significantly larger increase in plaque hyperechogenicity is most likely due to a change in plaque composition.

Impact of intravascular ultrasound guidance on directional coronary atherectomy.

In contrast to the luminogram of coronary angiography, intravascular ultrasound (IVUS) has proven to accurately assess both coronary lumen and vessel morphology due to its 360 degrees imaging capacity. Directional coronary atherectomy (DCA) improves the coronary lumen by removing plaque mass rather than stretching the vessel and compressing the plaque as with conventional percutaneous transluminal coronary angioplasty. In an attempt to optimize the procedural result of DCA we prospectively investigated the impact of IVUS guidance in a head to head comparison to on-line quantitative coronary angiography (QCA) on the result of DCA. In 16 consecutive patients IVUS demonstrated significant residual plaque mass after DCA irrespective of a satisfactory angiographic result. After a mean of 9 +/- 2 cuts luminal improvement was obtained with an area stenosis by angiography of 39 +/- 17% and by IVUS of 50 +/- 10% (p < 0.05), a diameter stenosis by angiography of 23 +/- 10% and IVUS of 35 +/- 14% (p < 0.05) and finally a minimal lumen diameter (MLD) by angiography of 2.9 +/- 0.5 mm and by IVUS of 2.3 +/- 0.5 mm (p < 0.005). After both on-line QCA and IVUS measurements a second series of 7 +/- 2 cuts were initiated to debulk more atheroma and improve stenosis dimensions. After additional cuts IVUS revealed further luminal improvement with an area stenosis by angiography of 25 +/- 16% and IVUS of 21 +/- 18% (n.s.), a diameter stenosis by angiography of 16 +/- 11% and by IVUS of 13 +/- 19% (n.s.) and finally a MLD by angiography of 3.1 +/- 0.5 mm and by IVUS of 2.8 +/- 0.3 mm (p < 0.05). Intraprocedural use of IVUS is superior to on-line QCA to assess the immediate result of DCA. IVUS-guided DCA results in more effective atheroma debulking than luminographic evaluation. Results of larger follow-up studies are needed to substantiate the intraprocedural advantage of IVUS with DCA.

Proximal aortic dissection late after aortic valve surgery: 119 cases of a distinct clinical entity.

BACKGROUND: Besides systemic hypertension and Marfan syndrome, only previous aortic valve replacement (AVR) is independently associated with proximal (type A) aortic dissection. Little, however, is known to date about the characteristic features of this clinical entity. METHODS: Clinical, prognostic and predisposing profiles in 119 cases of dissection and/or aneurysm occuring 1 month to 16 years after routine AVR were analyzed comprising 62 cases from our database and 57 reported cases. RESULTS: Dissection after AVR has been observed in 0.6% of all routine AVR procedures in the past four decades. With clinical signs, symptoms and anatomical features different from classic aortic dissection post-AVR dissection is a distinct clinical entity with a high intraoperative mortality of 44% and a 30-day and 5-year survival of 62% and 43%, respectively. Aortic regurgitation and a thin and/or fragile aortic wall at AVR, however, predict late dissection. Using a prediction model, the risk of late dissection can be stratified based on information obtained during AVR surgery. CONCLUSIONS: Aortic dissection following AVR is likely to represent a distinct clinical entity which can be predicted and possibly prevented at AVR.

[Acute results of ablation of coronary in-stent restenoses with eccentric excimer laser catheters]. / Akutergebnisse der Ablation koronarer In-Stent-Restenosen mit exzentrischen Excimer-Laserkathetern.

UNLABELLED: Laser catheters which run eccentrically on a guide wire were developed for maximization of luminal gain by excimer laser angioplasty (ELCA). We investigated the safety and efficacy of ELCA with these new catheters plus PTCA in patients with restenoses or occlusions in coronary stents. ELCA was performed in 57 patients (60 +/- 9 years) with stenoses in 75 stents (35 AVE Micro stents, 26 Palmaz-Schatz stents, 7 NIR stents, 7 other stents). In 44 patients eccentric 1.7 mm catheters and in 13 patients 2.0 mm catheters were used. The success of the intervention was analyzed by intravascular ultrasound (IVUS) in a subgroup of 7 patients treated with five 1.7 mm and two 2.0 mm catheters. The laser catheters could be advanced through the in-stent restenoses in 56 patients. A passage inhibition occurred in one patient with an inadequately expanded stent < 2.0 mm in diameter. ELCA reduced the diameter stenoses from 77 +/- 10% before intervention to 44 +/- 8% after treatment with the 1.7 mm catheter (n = 43) or to 34 +/- 9% after passages with the 2.0 mm catheter (P < 0.001). PTCA further reduced the diameter stenosis to 11 +/- 12% (P < 0.001). The IVUS analysis revealed a smooth ablation profile in all patients. In 4 patients creatine kinase elevations > or = 2 times normal value occurred. There was no evidence of a Q-wave infarction. No dissections were observed within the stents. Outside of the stents there were dissections in 5 vessels, which required the implantation of additional stents. CONCLUSIONS: ELCA with eccentric laser catheters for treatment of in-stent restenosis is safe and effective. The incidence of complications is acceptable.

Treatment of in-stent coronary restenosis by excimer laser angioplasty.

We evaluated the efficacy and safety of excimer laser angioplasty (ELCA) with adjunctive balloon angioplasty in patients with restenotic or occluded coronary stents. ELCA was performed in 70 patients (60 +/- 9 years), who had previously been treated with Micro Stents (n = 65), Palmaz-Schatz (n = 38), Wiktor, NIR, Freedom, and Multi-Link stents (n = 1 each). Restenosis (> or =50% diameter stenosis) was documented in 90 stents, another 17 stents were occluded. Laser energy was delivered to the lesions with catheters 1.4, 1.7 (eccentric), and 2.0 mm in diameter. Procedural success was controlled by intravascular ultrasound in a subgroup. Laser catheters crossed all restenotic or occluded stents and decreased diameter stenosis from 80 +/- 13% to 44 +/- 11% (p <0.001). Adjunctive balloon angioplasty further reduced diameter stenosis to 13 +/- 13% (p <0.001). In 13 patients with 21 stents, serial intravascular ultrasound imaging revealed a reduction of plaque area within the stent by 34 +/- 22% (from 4.2 +/- 1.8 mm2 to 2.7 +/- 1.1 mm2) after ELCA and a reduction by 65 +/- 16% (to 1.5 +/- 0.7 mm2) after balloon angioplasty (p <0.01). There were 4 patients with an increase of creatine kinase levels, 8 patients with major dissections (in 7 patients they were related to adjunctive balloon angioplasty), 1 patient with distal embolization, 2 with minor perforations, and 1 patient with stent dislocation. Reintervention during hospitalization was necessary in 3 patients. ELCA is an efficient and safe technique to debulk tissue in restenotic lesions and total occlusions within stents. The incidence of procedure related complications was low.

Echocardiographic diagnosis of papillary fibroelastoma of the mitral and tricuspid valve apparatus.

Papillary fibroelastomas are rare and normally benign cardiac tumors typically attached to cardiac valves. This report describes two patients who were evaluated for intermittent dyspnea in one case and for the source of cerebral embolism in the other. In both patients transthoracic echocardiography revealed a pedunculated mobile mass adjacent to an atrioventricular valve, suggestive of papillary fibroelastoma. Postoperative histology was confirmatory of papillary fibroelastoma with a typical hyalinized hypocellular stroma covered by a single layer of endocardial cells.

Radiofrequency current catheter ablation of accessory atrioventricular pathways in Ebstein's anomaly.

BACKGROUND: In patients with Ebstein's anomaly, localization of accessory pathways (APs) may be impeded by abnormal local electrograms recorded along the atrialized right ventricle and by the presence of multiple APs. The impact of these factors on radiofrequency (RF) current catheter ablation of APs has not been evaluated yet. METHODS AND RESULTS: Twenty-one patients with Ebstein's anomaly and reentrant atrioventricular tachycardias underwent electrophysiological evaluation and subsequent attempts at RF catheter ablation. Thirty-four right-sided APs were found, with 30 located along the atrialized ventricle. Local electrograms in this region were normal in 10 patients but fragmented in 11. Fragmented electrograms prevented the clear distinction between atrial and ventricular activation potentials as well as the identification of AP potentials. Right coronary artery mapping was performed in 7 patients. Abolition of all 26 APs was achieved in the 10 patients with normal local electrograms and in 6 of 11 patients with abnormal electrograms. Right coronary artery mapping allowed AP localization and ablation in 5 patients. In the 5 patients with abnormal electrograms and a total of 8 APs, 6 APs could not be ablated. Unsuccessfully treated patients received antiarrhythmic drugs. During 22 +/- 12 months of follow-up, 5 patients had clinical recurrences, including 4 who had undergone a successful RF procedure. CONCLUSIONS: In patients with Ebstein's anomaly and reentrant atrioventricular tachycardias, factors likely to account for failure of RF catheter ablation include an AP located along the atrialized right ventricle and the abnormal morphology of endocardial activation potentials generated in this region.

Radiofrequency catheter ablation of left atrial tachycardia originating within the pulmonary vein in a patient with dextrocardia.

A case is presented of a 38-year-old male with dextrocardia in whom radiofrequency current ablation of an incessant atrial tachycardia originating within the infero-lateral pulmonary vein was achieved. Activation mapping with detection of the earliest atrial activation was used for identification of the arrhythmogenic focus. In addition to fluoroscopy, transesophageal echocardiography was used for catheter guidance during the transseptal puncture. The present experience suggests that location of an arrhythmogenic focus within the pulmonary venous system should be considered whenever early atrial activation during ectopic atrial tachycardia is recorded at the junction between the left atrium and the pulmonary veins.

[Diastolic left ventricular dysfunction with microvascular angina (Syndrome X)]. / Diastolische linksventrikulare Dysfunktion bei Mikreovaskular-Angina (Syndrom X).

Findings on left ventricular function in microvascular angina (syndrome X) are somewhat controversial. Recently, an increased prevalence of insulin resistance and hyperlipoproteinemia has been demonstrated as well as arterial hypertension potentially impairing the left ventricular diastolic function. In an attempt to analyze the diastolic function at rest, we investigated by Doppler echocardiography the transmitral blood flow in 16 patients (51 +/- 8 years). The diastolic data were compared with those of 12 healthy people (50 +/- 6 years) who were matched for age. The patients with microvascular angina revealed a slightly higher systolic blood pressure (134 +/- 18 mm Hg vs 125 +/- 9 mm Hg, n.s.), but imposed by higher left ventricular mass index (92 +/- 18 g/m2 vs 65 +/- 13 g/m2, p < 0.001). There was a trend to an elevated A-wave-peak during transmitral blood flow (61 +/- 14 cm/s vs 50 +/- 9 cm/s). The findings suggest impairment of the left ventricular relaxation before manifestation of left ventricular hypertrophy and hypertension takes place.

Insulin resistance and hyperlipoproteinemia in microvascular angina: risk factors or pathogenetic link?

BACKGROUND: Patients with chest pain and normal epicardial coronary arteries (microvascular angina; syndrome X) are characterized by an impairment of myocardial perfusion reserve which may be related to functional and morphological abnormalities of the intramyocardial arterioles. METHODS: In an attempt to identify predisposing factors for microvascular angina we investigated 34 consecutive patients (15 female, 19 male; mean age 53 +/- 7 years) with microvascular angina but without hypertension or left ventricular hypertrophy. The metabolic profile, including plasma insulin, glucose, cholesterol, low-density lipoprotein cholesterol, triglycerides, very-low-density lipoprotein cholesterol and fibrinogen levels, was determined in each case. Furthermore, insulin and glucose levels were measured after an oral glucose load of 100 g over 3 h. All parameters were compared with those of a control group of 15 healthy subjects matched for age, sex and body mass index. RESULTS: The systolic blood pressure in microvascular angina was 137 +/- 17 mmHg and thus higher than that of healthy controls (124 +/- 11 mmHg); diastolic blood pressure was 85 +/- 7 compared with 78 +/- 9 mmHg in controls. Insulin level was significantly elevated in patients with microvascular angina 90 min (median: 101 versus 54 microU/ml) and 120 min (median: 88 versus 51 microU/ml) after ingestion of 100 g glucose. The fasting glucose level was 98 +/- 12 versus 87 +/- 7 mg/dl in controls. Glucose concentration was also elevated after 30 min (176 +/- 28 versus 148 +/- 32 mg/dl), after 45 min (198 +/- 35 versus 152 +/- 53 mg/dl) and after 60 min (193 +/- 44 versus 145 +/- 54 mg/dl). In microvascular angina, parameters such as total cholesterol (244 +/- 46 versus 199 +/- 29 mg/dl), low-density lipoprotein cholesterol (157 +/- 41 versus 122 +/- 18 mg/dl) and fibrinogen (377 +/- 150 versus 285 +/- 69 mg/dl) were elevated. CONCLUSIONS: The metabolic profile in patients with microvascular angina suggests a pathogenetic role of insulin resistance and hyperlipoproteinemia in the setting of impaired myocardial coronary reserve and in early stages of hypertensive heart disease.

[The significance of insulin resistance and hyperlipidemia in microvascular angina (syndrome X)]. / Die Bedeutung von Insulinresistenz und Hyperlipoproteinämie bei Mikrovaskular-Angina (Syndrom X).

Patients with chest pain and normal epicardial coronary arteries are characterized by an impairment of myocardial perfusion reserve. Functional and morphological abnormalities of the intramyocardial arterioles are suggested to be responsible for this, possibly as a consequence of hypertension and/or left ventricular hypertrophy. In an attempt to isolate predisposing factors of microvascular angina we investigated 34 patients (15 f, 19 m) with a mean age of 53 +/- 7 years. They were diagnosed as microvascular angina without hypertension or left ventricular hypertrophy. Parameters such as plasma insulin, glucose, cholesterol, LDL-cholesterol, triglycerides, (VLDL-cholesterol) and fibrinogen were determined for a metabolic profile. Furthermore, insulin and glucose were measured after an oral glucose load of 100 g glucose (OGTT) over 3 h. All parameters were compared to a control group of 15 healthy people matched for age and body mass index. In the study population systolic blood pressure was within normal limits at 137 +/- 17 mm Hg and thus higher than control at 124 +/- 11 mm Hg (p < 0.02). Furthermore, diastolic blood pressure was 85 +/- 7 mm Hg compared to 78 +/- 9 mm Hg in controls (p < 0.02). Insulin was significantly elevated in patients with microvascular angina 90 min (median: 101 vs 54 microU/ml; p < 0.01) and 120 min (median: 88 vs 51 microU/ml; p < 0.05) after ingestion of 100 g glucose. The fasting glucose was elevated at 98 +/- 12 compared to 87 +/- 7 mg/dl in controls (p < 0.01). Glucose concentration was also elevated after 30 min at 176 +/- 28 compared to 148 +/- 32 mg/dl (p < 0.02), after 45 minutes (198 +/- 35 compared to 152 +/- 53 mg/dl) (p < 0.01) and 60 minutes (193 +/- 44 compared to 145 +/- 54 mg/dl) (p < 0.01). In microvascular angina parameters such as total cholesterol: (244 +/- 46 vs 199 +/- 29 mg/dl (p < 0.01)), LDL-cholesterol (157 +/- 41 vs 122 +/- 18 mg/dl (p < 0.01)) and fibrinogen: (377 +/- 150 vs to 285 +/- 69 mg/dl (p < 0.03)) were elevated. These findings suggest a pathogenetic role of insulin resistance, hyperlipoproteinemia and elevated levels of fibrinogen for impaired myocardial coronary reserve. This metabolic constellation as well as exhaustion of coronary reserve is often found in hypertensive patients and may identify microvascular angina as an early stage of hypertensive heart disease before manifest hypertension has developed.