Cystamine slows but not inverses the progression of monocrotaline-induced pulmonary arterial hypertension in rats.

Tissue transglutaminase (TG2) plays an important role in pulmonary arterial hypertension (PAH). Previous research indicate that TG2 and protein serotonylation catalyzed by TG2 are upregulated in PAH. Serotonin transporter inhibitor fluoxetine ameliorates PAH via inhibition of protein serotonylation. It is still unknown whether PAH is inhibited through direct inhibition of TG2. Therefore, the present study aimed to investigate the effects of TG2 inhibitor cystamine on monocrotaline-induced PAH in rats. Rats were treated with monocrotaline (60 mg·kg-1, i.p.) in combination with or without cystamine (20, 40 mg·kg-1·day-1, p.o.). The results showed that compared with monocrotaline alone, combination of monocrotaline with cystamine (40 mg·kg-1·day-1, p.o.) relieved right ventricle hypertrophy, inhibited pulmonary arteriolar remodeling, and downregulated protein expression of TG2, phosphorylated protein kinase B (Akt), and extracellular regulated protein kinase (ERK) at day 21. However, except for TG2 expression, these changes were not significantly inhibited by cystamine at day 35. In addition, cystamine dose-dependently enhanced the survival rate of rats injected with monocrotaline at day 35. The findings suggest that cystamine slows but not reverses monocrotaline-induced PAH in rats, which was largely associated with the inhibition of TG2 protein expression and Akt and ERK activation.

Role of endocardial septal ablation in the treatment of hypertrophic obstructive cardiomyopathy.

Septal reduction therapy is accepted as a first therapeutic option for symptomatic drug-resistant hypertrophic obstructive cardiomyopathy (HOCM). Although, surgical septal myectomy is the gold standard method, alcohol septal ablation is a well-studied alternative approach in the patients with suitable anatomy. Endocardial septal ablation (ESA) therapy was relatively new defined modality and outcomes of the procedure were not clearly elucidated yet. We aimed to review the clinical aspects of ESA procedure and provide some historical background.

Subclinical Myocardial Impairment Occurred in Septal and Anterior LV Wall Segments After Anthracycline-Embedded Chemotherapy and did not Worsen During Adjuvant Trastuzumab Treatment in Breast Cancer Patients.

In a previous study of breast cancer patients, we found changes in cardiac function and size during the early stages of adjuvant trastuzumab (Herceptin(®)) therapy. Here we present a subgroup analysis of this patient cohort. This subgroup received a anthracycline-embedded chemotherapy followed by at least 3 months up to 6 months of adjuvant Herceptin(®) therapy. Twenty-seven female breast cancer patients with Her-2/-neu overexpression were studied using conventional echocardiography and 2D speckle tracking. These methods were done before anthracycline-embedded chemotherapy, before adjuvant trastuzumab therapy, and both 3 and 6 months after the start of the therapy (T3, T6). The LV-EF (Simpson biplane) decreased significantly from before the chemotherapy to after the chemotherapy and further decreased after 3 months of trastuzumab therapy (66.2 ± 1.5 vs. 58.7 ± 1.2 vs. 55.6 ± 1.3 vs. 55.9 ± 1.5 %; p < 0.05). The stroke volume index remained constant after chemotherapy (22.0 ± 0.8 vs. 22.6 ± 1.3 ml/m(2); p = 0.9), but increased significantly during trastuzumab therapy (26.7 ± 1.1 and 27.3 ± 1.0 ml/m(2); p < 0.01). Global longitudinal strain exclusively decreased during chemotherapy (-21.0 ± 0.5 vs. -18.9 ± 0.5 %, p < 0.001). Regional longitudinal strain decreased significantly after chemotherapy in septal, anteroseptal, anterolateral, and apex segments. Mitral valve regurgitation increased during the whole treatment, but especially during trastuzumab. Right ventricular function decreased exclusively during chemotherapy. Anthracycline-embedded chemotherapy in patients with breast cancer led to a decrease in LV function, especially of the septal and anterior segments, and did not worsen during adjuvant trastuzumab treatment.

Inaccuracy of transthoracic echocardiography for the identification of right-sided vegetation in patients with no history of intravenous drug abuse or cardiac device insertion.

OBJECTIVE: The use of transthoracic echocardiography (TTE) to identify right-sided infective endocarditis (RSIE) vegetation is controversial. Data are scarce for patients with no history of intravenous drug abuse (IVDA) or cardiac device insertion. This study analysed the consistency of presurgical echocardiographic results with surgical findings for vegetation identification, and the factors that influence accuracy of echocardiography. METHODS: This retrospective trial divided infective endocarditis (IE) patients into three subgroups according to the results of their presurgical TTE: left-sided native IE (LSNIE), left-sided prosthetic valve IE (LSPIE) and RSIE. The accuracy of TTE was tested by comparing vegetation (number and location), detected presurgery by TTE, with actual findings during surgery. RESULTS: In total, 416 patients were analysed, 322 with LSNIE, 31 with LSPIE and 63 with RSIE. Consistency between TTE findings and surgical results was lower in the RSIE group compared with the LSPIE and LSNIE groups. Consistency was lowered by the presence of vegetation in multiple locations and atypical distribution--both of which were increased in the RSIE group. The chance of vegetation in both sides of the heart rose with increased numbers of vegetation locations in RSIE patients. A high proportion of RSIE patients had congenital heart defects, mostly ventricular septal defects. CONCLUSIONS: TTE may be unsuitable for RSIE patients with no history of IVDA or cardiac device insertion, because multifocal and atypically distributed vegetation may influence detection accuracy.

Salivary biomarkers associated with myocardial necrosis: results from an alcohol septal ablation model.

OBJECTIVE: To determine if salivary biomarkers demonstrate utility for identifying aspects of myocardial necrosis. METHODS: Twenty-one patients undergoing alcohol septal ablation (ASA) for treatment of hypertrophic cardiomyopathy provided serum and unstimulated whole saliva at baseline and incremental time points post-ASA. Samples were analyzed for seven biomarkers related to myocardial damage, inflammation, and tissue remodeling using immunosorbent assays. Levels were compared with baseline and levels observed in 97 healthy controls. RESULTS: Biomarkers of myocardial damage and inflammation (ie, troponin I, creatine kinase-MB, myoglobin, C-reactive protein) rose in serum 2- to 812-fold after ASA (P < .01). Significant elevations of 2.0- to 3.5-fold were observed with C-reactive protein and troponin I in saliva (P < .02). Significant correlations between levels in serum and saliva were observed for C-reactive protein, matrix metalloproteinase-9, and myeloperoxidase (P < .001). CONCLUSIONS: Select salivary biomarkers reflect changes that occur during, and subsequent to, myocardial necrosis caused by ASA.

Coronary morphology and conduction system disturbance induced by therapeutic embolization of the coronary septal artery.

BACKGROUND: Percutaneous transluminal septal myocardial alcohol ablation (PTSMAA) is not a procedure without complications. It may produce heart arrhythmias, especially those due to disturbances of atrioventricular (AV) and interventricular (IV) electrical conduction. OBJECTIVE: The goal of this study was to evaluate the relationship between the anatomical patterns of the right coronary artery and the left anterior descending artery (LAD) and to relate them to the AV and IV bundle branch blocks provoked by PTSMAA. METHOD: Twenty patients with obstructive hypertrophic cardiomyopathy resistant to treatment with drugs successfully underwent PTSMAA. Electrocardiographic analyses were done before and after PTSMAA, and the results were compared with the abnormal septal anatomy. RESULTS: The effectiveness of PTSMAA was obtained in 18 (90%) of the 20 patients by ethanolization of the first great septal branch. In the other 2 patients (10%), 2 septal branches underwent alcoholization. First-grade temporary AV block (AVB) was observed in 6 patients (30%). Ten patients experienced severe bradycardia due to total AVB that required a temporary pacemaker, but 3 of the patients (15%) required a permanent pacemaker. Fourteen patients (70%) experienced permanent complete right branch block, and 2 developed incomplete left anterior block and incomplete left posterior block. Six patients presented with no electrical conduction disturbance at all. CONCLUSION: According to the results of the present investigation with the AV node artery derived from the right coronary artery in all cases, complete and permanent AV conduction system blockade occurred after PTSMAA in all types of anatomy regarding the observed LAD.

Late in-hospital pressure gradient measurements improve prediction of long-term outcome of alcohol septal ablation in hypertrophic cardiomyopathy.

BACKGROUND: Left ventricular outflow gradient is associated with increased morbidity and mortality in hypertrophic cardiomyopathy. Alcohol septal ablation is the alternative to surgery in cases refractory to drug therapy. The implication of LVOG measured 1 week post-ASA for prediction of outcome is unknown. OBJECTIVE: To observe the pattern of LVOG course and prediction of long-term clinical and hemodynamic outcome of ASA. METHODS: Baseline clinical and echocardiographic parameters were prospectively recorded in 14 consecutive patients with a first ASA, at the time of ASA, 3 and 7 days after ASA (in-hospital), and 3 and > or = 12 months after ASA (last follow-up). RESULTS: There was improvement in NYHA class, exercise parameters and LVOG in 11 of 14 patients (P < 0.005 in all). Maximal creatine kinase level was lower than 500 U/L in those without such improvement and 850 U/L or higher in successful cases. LVOG dropped from 79 +/- 30 to 19 +/- 6 mmHg after the ASA. LVOG was 50 +/- 21 mmHg on day 3, 39 +/- 26 on day 7, 32 +/- 26 at 3 months and 24 +/- 20 mmHg at last follow-up. LVOG identified 27% sustained procedural successes on day 3 and 73% on day 7. The overall predictive accuracy of the test for sustained success and failure was 36% on day 3 and 71% on day 7. Combination of maximal CK and LVOG on day 7 showed four distinct outcome patterns: "early success" with low LVOG and high CK (73% of successful cases), "late success" with high LVOG and high CK, and "early failure" and "late failure" with both low CK and high or low LVOG, respectively. CONCLUSION: LVOG measurement 7 days post-ASA combined with maximal CK levels predicts late procedural outcome in the majority of patients.

Aldosterone receptor antagonists induce favorable cardiac remodeling in diastolic heart failure patients / Antagonistas de receptores de aldosterona inducen remodelación cardiaca favorable en pacientes con insuficiencia cardiaca diastólica

Background. Serum levels of aldosterone in heart failure are increased up to 20 times compared to normal subjects. After an acute myocardial infarction, aldosterone increases progressively as well as interstitial fibrosis and collagen synthesis from cardiac fibroblasts, forming a patchy heterogeneous interstitial collagen matrix that affects ventricular function. Even if angiotensine converting enzyme inhibitors (ACEI) or angiotensin II receptor antagonists (ARA) can reduce aldosterone levels early during treatment, they increase again after a 12 week treatment. The aim of this study was to evaluate the changes in structure and function of the left ventricle in symptomatic (NYHA I-III) diastolic heart failure patients receiving an aldosterone receptor antagonist. Methods. Twenty-eight subjects with diastolic heart failure, on BB, ACEI and/or ARA were randomized to receive spironolactone (group A) on a mean dose of 37.5 mg once a day (n =14, age 63.7 ± 21.6 years and body mass index, BMI 27.5 ± 9.4), or not (group B, n = 14, Age 64.8 ± 11.9, BMI 26.9 ± 4.7). All patients were followed-up for a mean of 13.79 ± 0.99 months. Results. Group A showed a 42.8% ischemic origin of heart failure, while in group B was 55% (p = 0.2). No other co-morbidities were significativelly different among both groups. Mean percentage of changes by echocardiogram was as follows: Interventricular septum (IVS) -12.2 ± 11% vs. 1.3 ± 15.2 (p = 0.03), pulmonary systolic artery pressure (PSAP was 0.99 ± 3.8% vs. 10.5 ± 9.1, p = 0.05). Other parameters did not show statistically significant differences. Conclusion. Aldosterone receptor antagonists reduce or avoid increasing of PSAP and inducing a favorable remodeling of the left ventricle, especially in the IVS in diastolic heart failure patients.

Antecedentes. En pacientes con insuficiencia cardiaca existen aumentos de aldosterona hasta 20 veces mayores que en sujetos control. Después de un infarto miocárdico la aldosterona aumenta progresivamente, así como la fibrosis intersticial y la síntesis de colágena por fibroblastos cardiacos, provocando parches intersticiales heterogéneos en la matriz de colágena que afecta la función ventricular. El tratamiento inicial con inhibidores de enzima convertidora de angiotensina (IECA) y/o antagonistas de receptores de angiotensina II (ARA) puede reducir estos niveles; sin embargo, aumentan nuevamente después de 12 semanas de tratamiento. El propósito de este estudio fue evaluar los cambios estructurales y funcionales en el ventrículo izquierdo en pacientes con insuficiencia diastólica tratados con ARA angiotensina (NYHAI-III). Métodos. Veintiocho pacientes con insuficiencia cardiaca diastólica en tratamiento con BB, IECA y/o ARA se aleatorizaron a recibir una dosis media de 37.5 mg una vez al día de espironolactona (grupo A) (n - 14, edad 63.7 ± 0 21.6 años e índice masa corporal IMC 27.5 ± 9.4), o no (grupo B, n =14, edad 64.8 ± 11.9, IMC 26.9 ± 4.7). Todos los pacientes fueron seguidos por 13.79 ± 0.99 meses. Resultados. De los pacientes del grupo A, 42.8% y el 55 del grupo B (p = 0.2), tenían cardiopatía isquémica. No se encontraron diferencias significativas en otras comorbilidades. El porcentaje promedio de cambios en el ecocardiograma se observó en septum interventricular (SIV) -12.2 ± 11% vs. 1.3 ± 15.3% (p = 0.02), y la presión sistólica de la arteria pulmonar (PSAP, 0.99 ± 3.8% vs. 10.5 ± 9.1, p = 0.05, para los grupos A y B, respectivamente). Los otros parámetros no mostraron diferencias estadísticamente significativas. Conclusión. El tratamiento con antagonistas de receptores de aldosterona disminuye o limita aumentos de PSAP e inducen una remodelación favorable del ventrículo izquierdo, especialmente del SIV en pacientes con insuficiencia cardiaca diastólica.

Eosinophilic myocarditis presenting with pediatric myocardial infarction.

Determination of the etiology of myocardial infarction (MI) in children can present a challenge to the practitioner since cases of pediatric MI are rare and the causes can be diverse. We report an unusual case of pediatric eosinophilic myocarditis that presented with MI.

Ultrasound tissue characterization by integrated backscatter for analyzing Fluorouracil induced myocardial damage.

BACKGROUND: 5-Fluorouracil (5-FU) cardiotoxicity is a well-known clinical phenomenon whose pathophysiology remains controversial. Cyclic variation of integrated backscatter (CVIBS) assesses acoustic properties of myocardium that may reflect both contractility and structural changes. The aim of this study was to evaluate CVIBS alterations in cancer patients under high-dose leucovorin and infusional 5-FU (HDLV5FU) chemotherapy. METHOD: We prospectively evaluated 37 cancer patients under HDLV5FU treatment. Transthoracic echocardiography and CVIBS were performed at the 0th, 48th hours, and on day 15 of the first cycle. The parasternal long-axis view was preferred to obtain the image of integrated backscatter and mainly two regions of interest--interventricular septum (IVS) and posterior wall (PW)--were used. RESULTS: Clinical cardiotoxicity was observed in two patients. No significant differences were detected in pre- and posttreatment conventional echocardiography evaluations. However, both the IVS (9.3 +/- 1.0 to 8.1 +/- 1.2 dB, P < 0.001) and PW (9.1 +/- 0.7 to 7.8 +/- 0.9 dB, P < 0.001) CVIBS values significantly decreased in all patients. All values were returned to pretreatment levels (9.2 +/- 0.9 dB in the CVIBS-IVS and 8.9 +/- 0.6 dB in CVIBS-PW, respectively) on day 15 after the treatments. CONCLUSION: This study suggests that HDLV5FU may cause acute transient alterations in CVIBS values in the absence of clinical symptoms and signs of cardiotoxicity. The clinical value of CVIBS should be further studied in patients receiving 5-FU-based therapy.

Lack of prognostic value of normalized integrated backscatter analysis of myocardium in patients with thalassemia major: a long-term follow-up study.

BACKGROUND: Patients with beta-thalassemia major often present with severe anemia and must undergo continuous transfusion therapy, consequently developing iron overload leading to hemochromatosis. Because of these the iron deposits and/or secondary structural changes, patients develop an increase in myocardial integrated backscatter (IB). AIM: To investigate the prognostic value of analyzing acoustic quantitative properties of the myocardium in patients with beta-thalassemia major. PATIENTS AND METHODS: Between 1989 and 1990, 38 patients (mean age: 18 years, range: 7-26, 21 males) with beta-thalassemia major and without clinical signs of cardiac failure were enrolled prospectively. All patients were on chelation therapy (desferroxiamine). To obtain quantitative operator-independent measurement of the IB signal of the left ventricular septum and posterior wall, the ultrasonic radiofrequency signal integrated values were normalized to the pericardial interface and expressed in percentage (IB%). RESULTS: Follow-up was 122 +/- 36 months, during which 15 events (7 cardiac deaths and 8 heart failures) occurred. The event-free survival was comparable in patients with normal and abnormal IB%. Septal IB% was 33 +/- 14 in the 15 patients with events, and 33 +/- 12 in the 25 patients without events (P = ns). The %IB had no prognostic value in this population. A prognostic value was found in multivariate analysis for patient refusal/noncompliance of chelation therapy (P = 0.02, OR: 4.37, 95% CI: 1.72-16.9) and also body mass index (P = 0.04, OR: 1.2, 95% CI: 1.0-1.4). CONCLUSION: Analysis of end-diastolic IB% of myocardium in patients with beta-thalassemia and iron overload was not predictive of adverse cardiac events during long-term follow-up in this study.

Adenoviral-mediated transfer of vascular endothelial growth factor 121 cDNA enhances myocardial perfusion and exercise performance in the nonischemic state.

BACKGROUND: Angiogenic gene therapy has been demonstrated to enhance perfusion to ischemic tissues, but it is unknown whether the administration of angiogenic growth factors will increase blood flow to nonischemic tissues. This study investigates whether enhanced myocardial perfusion can be mediated by adenovirus-mediated transfer of vascular endothelial growth factor 121 cDNA to nonischemic myocardium. METHODS: New Zealand White rabbits received adenovirus (5 x 10(10) particle units) encoding for vascular endothelial growth factor 121 (n = 14) or a control vector without a transgene (n = 13) or saline solution (n = 9) via direct myocardial injection. Fluorescent microsphere perfusion studies and histologic analyses were performed 4 weeks later. In a parallel study, exercise treadmill testing was performed to assess the functional effects of this therapy in Sprague-Dawley rats. RESULTS: Microsphere assessment of myocardial perfusion in rabbits 4 weeks after adenovirus-encoding vascular endothelial growth factor administration was greater than that for rats injected with control vector without a transgene or saline solution (3.2 +/- 0.5 vs 2.7 +/- 0.7 and 2.4 +/- 0.4, respectively; P <.03). The endothelial cell count per high power field was increased in animals injected with adenovirus-encoding vascular endothelial growth factor versus animals injected with control vector without a transgene or saline solution (147 +/- 27 vs 123 +/- 14 and 125 +/- 16 cells, respectively), although this did not reach statistical significance (P =.12). Rats treated with adenovirus-encoding vascular endothelial growth factor also demonstrated prolonged exercise tolerance compared with rats injected with control vector without a transgene or saline solution (exhaustion time: 26 +/- 5 minutes vs 19 +/- 2 minutes and 20 +/- 3 minutes, respectively; P =.006). CONCLUSIONS: Adenovirus encoding-mediated transfer of vascular endothelial growth factor 121 induces an enhancement in regional perfusion in nonischemic myocardium that corresponds to changes in exercise tolerance. Adenovirus-encoding vascular endothelial growth factor therapy may be useful for inducing angiogenesis in the nonischemic state, such as for prophylactic therapy of early coronary artery disease.

Vector electrocardiographic alterations after percutaneous septal ablation in obstructive hypertrophic cardiomyopathy. Possible anatomic causes.

OBJECTIVE: Analyze the dromotropic disturbances (vector-electrocardiographic), and the possible anatomic causes, provoked by selective alcohol injection in the septal branch, for percutaneous treatment, of obstructive hypertrophic cardiomyopathy. METHODS: Ten patients with a mean age of 52.7 years underwent percutaneous septal ablation (PTSA) from october 1998; all in functional class III/IV). Twelve-lead electrocardiogram was performed prior to and during PTSA, and later electrocardiogram and vectorcardiogram according to Frank's method. The patients were followed up for 32 months. RESULTS: On electrocardiogram (ECG) prior to PTSA all patients had sinus rhythm and left atrial enlargement, 8 left ventricular hypertrophy of systolic pattern. On ECG immediately after PTSA, 8 had complete right bundle-branch block; 1 transient total atrioventricular block; 1 alternating transient bundle-branch block either right or hemiblock. On late ECG 8 had complete right bundle-branch block confirmed by vectorcardiogram, type 1 or Grishman. CONCLUSION: Septal fibrosis following alcohol injection caused a predominance of complete right bundle-branch block, different from surgery of myotomy/myectomy.

Clinical and electrophysiologic characteristics of left septal atrial tachycardia.

OBJECTIVES: It was the purpose of this study to define the electrophysiologic (EP) identity of left septal atrial tachycardia (AT). BACKGROUND: The clinical and EP characteristics of this particular type of arrhythmia have not been fully described. METHODS: A total of 120 patients with AT underwent invasive EP evaluation. Five patients (two men and three women; mean age 49 +/- 15 years) with left septal AT were identified. Mapping of the right and left atrium was performed using conventional electrode catheters (five patients) and a three-dimensional electroanatomic mapping system (three patients) followed by radiofrequency (RF) ablation at the earliest site of local endocardial activation. RESULTS: Five tachycardias with a mean cycle length of 320 +/- 94 ms were mapped, and the earliest endocardial electrogram occurred 22 +/- 10 ms before the onset of the surface P-wave. Three left septal ATs were found to be originating from the left inferoposterior atrial septum and two from the left midseptum. During tachycardia, positive (three patients), biphasic negative-positive deflection (one patient), or isoelectric (one patient) P waves were recorded in lead V(1). The inferior leads demonstrated a positive or biphasic P-wave morphology in four of five patients (80%). Four patients were given both adenosine and verapamil during AT. In three of four patients, verapamil successfully terminated AT after adenosine had failed. Adenosine successfully terminated AT in one of four patients. Successful RF ablation was performed in all patients (mean 2.2 +/- 1.7 RF applications) without affecting atrioventricular conduction properties. No recurrence of AT was observed after a mean follow-up of 14 +/- 8 months. CONCLUSION: Left septal AT ablation is safe and effective. There was no consistent P-wave morphology associated with this particular type of AT. This arrhythmia appears to be resistant to adenosine and moderately responsive to calcium antagonists.

Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy. A comparison of clinical, haemodynamic and exercise outcomes.

AIMS: Surgical myectomy has been successfully used to treat patients with symptomatic obstructive hypertrophic cardiomyopathy (HCM). More recently, alcohol septal ablation has been advocated as a less invasive, but equally effective alternative therapy. The aim of this non-randomized cohort study was to compare subjective and objective outcomes in patients undergoing these therapies. METHODS: Forty-four patients (25 male; age 41+/-15 years) with symptomatic drug-refractory obstructive HCM were studied. Twenty-four patients underwent surgical myectomy and 20 alcohol septal ablation. All patients underwent clinical evaluation, echocardiography and upright maximal cardiopulmonary exercise testing using a cycle ergometer before and following their intervention. RESULTS: Peak gradient was reduced to a similar extent by both modalities (myectomy: 83+/-23 to 15+/-10 mmHg (P<0.000001); ablation: 91+/-18 to 22+/-14 mmHg (P<0.000002);P =0.48 for myectomy vs ablation) and led to similar improvements in NYHA class (myectomy: 2.4+/-0.6 to 1.5+/-0.7 (P<0.00001); ablation: 2.3+/-0.5 to 1.7+/-0.8 (P<0.0001);P=0.3 for myectomy vs ablation). Myectomy resulted in a greater improvement in peak oxygen consumption (myectomy: 16.4+/-5.8 to 23.1+/-7.1 ml.kg(-1) min(-1) (P<0.00002); ablation: 16.2+/-5.2 to 19.3+/-6.1 ml.kg(-1) min(-1) (P<0.05);P <0.05 for myectomy vs ablation) and work rate achieved (myectomy: 130+/-57 to 161+/-60 watts (P<0.04); ablation: 121+/-53 to 137+/-51 watts (P=0.11);P <0.05 for myectomy vs ablation). CONCLUSION: Surgical myectomy and alcohol septal ablation are equally effective at reducing obstruction and subjective exercise limitation in appropriately selected patients. However, the superior effect of surgical myectomy on exercise test parameters suggests that surgery remains the gold standard against which new treatment modalities should be compared.

Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy.

OBJECTIVES: This study was designed to compare the hemodynamic efficacy of nonsurgical septal reduction therapy (NSRT) by intracoronary ethanol with standard therapy (surgical myectomy) for the treatment of hypertrophic obstructive cardiomyopathy (HOCM). BACKGROUND: Nonsurgical septal reduction therapy has gained interest as a new treatment modality for patients with drug-refractory symptoms of HOCM; however, its benefits in comparison to surgery are unknown. METHODS: Forty-one consecutive NSRT patients at Baylor College of Medicine with one-year follow-up were compared with age- and gradient-matched septal myectomy patients at the Mayo Clinic. All patients had left ventricular outflow obstruction with a resting gradient > or =40 mm Hg and none had concomitant procedures. RESULTS: There were no baseline differences in New York Heart Association class, severity of mitral regurgitation, use of cardiac medications or exercise capacity. One death occurred during NSRT because of dissection of the left anterior descending artery. At one year, all improvements in both groups were similar. After surgical myectomy, more patients were on medications (p < 0.05) and there was a higher incidence of mild aortic regurgitation (p < 0.05). After NSRT, the incidence of pacemaker implantation for complete heart block was higher (22% vs. 2% in surgery; p = 0.02). However, seven of the nine pacemakers in the NSRT group were implanted before a modified ethanol injection technique and the use of contrast echocardiography. CONCLUSIONS: Nonsurgical septal reduction therapy resulted in a significantly higher incidence of complete heart block, but the risk was reduced with contrast echocardiography and slow ethanol injection. Surgical myectomy resulted in a significantly higher incidence of mild aortic regurgitation. Nonsurgical septal reduction therapy, guided by contrast echocardiography, is an effective procedure for treating patients with HOCM. The hemodynamic and functional improvements at one year are similar to those of surgical myectomy.

Percutaneous transluminal alcohol septal myocardial ablation after aortic valve replacement.

When left ventricular outflow tract obstruction develops after aortic valve replacement, few treatment choices have been available until now. We present a patient with prior aortic valve replacement who developed left ventricle outflow tract obstruction that was successfully treated with a percutaneous transcoronary myocardial septal alcohol ablation. This technique is a useful tool for the treatment of obstructive hypertrophic cardiomyopathy, especially in those patients with prior heart surgery.

Percutaneous transluminal septal myocardial ablation in drug-resistant hypertrophic obstructive cardiomyopathy: 18-month follow-up results.

OBJECTIVE: Surgery has been the only therapeutic option in patients with hypertrophic obstructive cardiomyopathy (HOCM) who are resistant to standard treatment. Percutaneous transluminal septal myocardial ablation (PTSMA) by alcohol-induced occlusion of the septal artery for the reduction of left ventricular outflow tract (LVOT) gradient is a novel method. However, long-term clinical follow-up is insufficient. This study reports the acute and mid-term results after PTSMA in symptomatic patients with HOCM. METHODS: Six patients (4 men and 2 women) with symptomatic HOCM and inadequate response to pharmacologic therapy had their major septal branches ablated with alcohol. Mean duration of follow-up was 1.5 years. RESULTS: There was reduction in LVOT gradient in all patients (100%) with a mean reduction of 50 mmHg. Two patients developed complete heart block (CHB) and 3 patients developed bifascicular block. CHB persisted in 1 patient. Two patients died within 8 days of the procedure; one due to cerebrovascular accident and 1 due to asystole. The patient who died of asystole had CHB but refused permanent pacemaker implantation. CHB reverted in 1 patient and bifascicular blocks persisted in 3 patients. Clinical and echocardiographic follow-up was achieved in the 4 surviving patients after 1.5 years. All surviving patients had LVOT gradient reduction and clinical improvement. CONCLUSION: PTSMA for HOCM is a non-surgical technique for reducing LVOT gradient. Heart blocks are one potential complication, and may require pacemaker implantation. Long-term follow-up and a larger series of patients are required to determine conclusive therapeutic significance.

Adenosine induced ventricular arrhythmias in the emergency room.

While adenosine effectively terminates most supraventricular tachycardias (SVT), rare case reports have demonstrated its proarrhythmic potential, including induction of ventricular tachycardia (VT). The aim of this study was to define the proarrhythmic effects of adenosine in a large, unselected population. During a 5-year period, adenosine was used (average dose 9.7 mg) in the emergency room to manage 187 episodes of tachycardia in 127 patients. In two thirds of the cases, adenosine induced ventricular ectopy following successful termination of SVT, including premature ventricular complexes (PVC) and nonsustained VT. The adenosine induced PVCs and VT were transient and self-terminating. More than half had a right bundle branch block morphology with a superior axis that suggested an origin in the inferior left ventricular septum. In conclusion, although adenosine is commonly used in clinical practice to treat SVTs, we found that it induced PVCs and VT in two thirds of the patients. The high incidence of ventricular arrhythmias following adenosine infusion was surprising but did not require further intervention. These arrhythmias appeared to frequently originate from the inferior left ventricular septum, suggesting that this area may be particularly susceptible to the proarrhythmic effects of adenosine.