Does ablation of atrial fibrillation at the time of septal myectomy improve survival of patients with obstructive hypertrophic cardiomyopathy?

ObjectiveTo evaluate the outcomes after septal myectomy in patients with obstructive hypertrophic cardiomyopathy according to atrial fibrillation and surgical ablation of atrial fibrillation.MethodsWe reviewed patients with obstructive hypertrophic cardiomyopathy who underwent septal myectomy at the Mayo Clinic from 2001 to 2016. History of atrial fibrillation was obtained from patient histories and electrocardiograms. All-cause mortality was the primary end point.ResultsA total of 2023 patients underwent septal myectomy, of whom 394 (19.5%) had at least 1 episode of atrial fibrillation preoperatively. Among patients with atrial fibrillation, 76 (19.3%) had only 1 known episode, 278 (70.6%) had recurrent paroxysmal atrial fibrillation, and 40 (10.2%) had persistent atrial fibrillation. Surgical ablation was performed in 190 patients at the time of septal myectomy, including 148 with pulmonary vein isolation and 42 with the classic maze procedure. Among all patients, operative mortality was 0.4%, and there were no early deaths in patients undergoing surgical ablation. Over a median follow-up of 5.6 years, patients with preoperative atrial fibrillation had increased mortality (hazard ratio, 1.36; 95% confidence interval, 0.97-1.91; P = .070) after multivariable adjustment for comorbidities. When considering the impact of atrial fibrillation with or without surgical treatment, the adjusted hazard ratio for mortality in patients undergoing ablation compared with no ablation was 0.93 (95% confidence interval, 0.52-1.69; P = .824).ConclusionsAtrial fibrillation is present preoperatively in one-fifth of patients with obstructive hypertrophic cardiomyopathy undergoing myectomy and showed a trend toward higher all-cause mortality. Survival of patients undergoing septal myectomy with preoperative atrial fibrillation was similar between those who did and did not receive concomitant surgical ablation.     

活体大蒜及离体蒜苗对连作当归胁迫的影响

目的:通过活体大蒜(garlic)及离体蒜苗(garlic sprout)挥发物对当归(Angelica sinensis)的化感效应,探索大蒜挥发性物质对连作当归存在的化感效应,为当归大蒜间作模式缓解连作当归胁迫提供一定的理论依据。方法:试验通过对当归各生长指标及叶片保护酶系统的测定分析,讨论当归在活体大蒜及离体蒜苗挥发物的影响作用下对连作胁迫、无连作胁迫环境的适应性及抗性生长发育机制。结果:整体分析,连作胁迫条件下离体蒜苗对当归幼苗化感效应处理(DC2)下的当归生长指标、叶片保护酶活性较当归单作(CK1)整体提高17. 51%,48. 34%;连作茬口种植活体蒜苗与当归间作处理(LC2)下的当归生长指标、叶片保护酶活性较当归单作(CK2)整体提高16. 63%,36. 65%;即离体蒜苗挥发物较活体大蒜缓解当归连作胁迫作用更显著。结论:无论有无连作障碍胁迫,适当浓度的活体大蒜及离体蒜苗挥发物对当归生长指标及叶片保护酶活性均表现为明显的化感促进作用,其化感促进作用在有连作胁迫条件下表现更显著,因而间作大蒜对当归连作障碍胁迫有一定的缓解作用。     

Gargantuan Left Atrium: A Sequela of Mitral Regurgitation and Mitral Stenosis

Cardiac magnetic resonance imaging and echocardiography revealed a gargantuan left atrium measuring 18.9 cm × 15.7 cm × 11.3 cm in a 56‐year‐old patient diagnosed with severe rheumatic mitral stenosis, severe pulmonary hypertension, and permanent atrial fibrillation. A chest x‐ray also revealed a cardiothoracic ratio approaching 1.0 and a transthoracic echocardiogram measured diameters as large as 19.2 cm. The patient then underwent mitral valve replacement and left atrial reduction surgery and has had no further admissions or complications.     

First-in-Man Experience with a Novel Catheter-Based Renal Denervation System of Ultrasonic Ablation in Patients with Resistant Hypertension

Purpose

To report results of renal denervation (RDN) with the first catheter-based, non–balloon occlusion ultrasonic system in patients with resistant hypertension.

Transesophageal Echocardiographic Diagnosis of Left Atrial Wall Dehiscene

Six months following Carbomedics mitral and aortic valve replacement, multiplane transesophageal echocardiography performed (TEE) in a 49-year-old black gentleman showed a prominent 1.0-cm linear echo protruding into the left atrium at the mid-interatrial septal level distal to the sewing ring. Plane angulations at 105 and 111 degrees demonstrated the linear echo to be related to left atrial wall dehiscence indicated by the presence of a cavitary defect at the same level. At the time of surgery, a 1.0 cm-paravalvular defect and dehiscence of the left atrial wall distal to the sewing ring 2.0 centimeters anterior to the posteromedial commisure were found.     

Transesophageal Echocardiographic Study of Right Atrial Myocardial Infarction and Myocardial Viability

In order to determine the effects of dobutamine on right atrial wall movement, two groups were studied using transesophageal echocardiography. Group A included six patients without ischemic heart disease. Group B included six patients with infarction of the inferior wall of both ventricles and abnormal wall movement of the right atrium. In group A, an increase in the amplitude of right atrial movement was observed with dobutamine at doses of 5 and 10 μ/kg per minute. In group B, infusion of dobutamine did not modify wall akinesis in three patients with right atrial infarction; in the remaining three, alterations of segmental atrial movement were evident, and their responses to dobutamine were related to the patency of right atrial coronary branches. The following conclusions were reached: (1) dobutamine has a positive inotropic effect on atrial myocardium; (2) right atrial ischemia appears in the echocardiogram as altered segmental or global wall movement; (3) dobutamine can be used in the evaluation of atrial myocardial viability.     

Uveoscleral Outflow in Dog's Eye: Role of Several Enzymes

The morphological pattern of several enzymes (succinic dehydrogenase – SDH, glucose-6-phosphate dehydrogenase – G6PDH and lactic dehydrogenase – LDH) was evaluated in normal dog eyes. Special attention was paid to the uveo-scleral tissue. Cryostatic sections of dog eye were stained with toluidine blue for the recognition of the microanatomical details or with histoenzymatic methods for SDH, G6PDH and LDH activities using sodium succinate, glucose-6-phosphate and sodium lactate as substrates respectively, nicotinamide adenine dinucleotide (NAD) as a reducing agent and sodium nitro-blue-tetrazolium as a colouring substance. A moderate positive reaction for SDH and a strong positive reaction for LDH were observed in the uveo-scleral tissue, while G6PDH gave negative staining. Some considerations regarding a possible active role of these enzymatic activities to the aqueous humor outflow are suggested. This revised version was published online in July 2006 with corrections to the Cover Date.     

Inhibitory effect of N-nitro-

1. The role of protein kinase C (PKC) in mediating the action of κ-receptor stimulation on intracellular Ca²⁺ and cyclic AMP production was determined by studying the effects of trans-(±)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl] cyclohexyl) benzeneacetamide methanesulphonate (U50,488H), a selective κ-receptor agonist, and phorbol 12-myristate 13-acetate (PMA), a PKC agonist, on the electrically-induced [Ca²⁺]_i transient and forskolin-stimulated cyclic AMP accumulation in the presence and absence of a PKC antagonist, staurosporine or chelerythrine, in the single rat ventricular myocyte.
2. U50,488H at 2.5–40 μM decreased both the electrically-induced [Ca²⁺]_i transient and forskolin-stimulated cyclic AMP accumulation dose-dependently, effects which PMA mimicked. The effects of the κ-agonist, that were blocked by a selective κ-antagonist, nor-binaltorphimine, were significantly antagonized by the PKC antagonists, staurosporine and/or chelerythrine. The results indicate that PKC mediates the actions of κ-receptor stimulation.
3. To determine whether the action of PKC was at the sarcoplasmic reticulum (SR) or not, the [Ca²⁺]_i transient induced by caffeine, that depletes the SR of Ca²⁺, was used as an indicator of Ca²⁺ content in the SR. The caffeine-induced [Ca²⁺]_i transient was significantly reduced by U50,488H at 20 μM. This effect of U50,488H on caffeine-induced [Ca²⁺]_i transient was significantly attenuated by 1 μM chelerythrine, indicating that the action of PKC involves mobilization of Ca²⁺ from the SR. When the increase in IP₃ production in response to κ-receptor stimulation with U50,488H in the ventricular myocyte was determined, the effect of U50,488H was the same in the presence and absence of staurosporine, suggesting that the effect of PKC activation subsequent to κ-receptor stimulation does not involve IP₃. The observations suggest that PKC may act directly at the SR.
4. In conclusion, the present study has provided evidence for the first time that PKC may be involved in the action of κ-receptor stimulation on Ca²⁺ in the SR and cyclic AMP production, both of which play an essential role in Ca²⁺ homeostasis in the heart.

     

Effects of κ-opioid receptor stimulation in the heart and the involvement of protein kinase C

1. The role of protein kinase C (PKC) in mediating the action of κ-receptor stimulation on intracellular Ca²⁺ and cyclic AMP production was determined by studying the effects of trans-(±)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl] cyclohexyl) benzeneacetamide methanesulphonate (U50,488H), a selective κ-receptor agonist, and phorbol 12-myristate 13-acetate (PMA), a PKC agonist, on the electrically-induced [Ca²⁺]_i transient and forskolin-stimulated cyclic AMP accumulation in the presence and absence of a PKC antagonist, staurosporine or chelerythrine, in the single rat ventricular myocyte.
2. U50,488H at 2.5–40 μM decreased both the electrically-induced [Ca²⁺]_i transient and forskolin-stimulated cyclic AMP accumulation dose-dependently, effects which PMA mimicked. The effects of the κ-agonist, that were blocked by a selective κ-antagonist, nor-binaltorphimine, were significantly antagonized by the PKC antagonists, staurosporine and/or chelerythrine. The results indicate that PKC mediates the actions of κ-receptor stimulation.
3. To determine whether the action of PKC was at the sarcoplasmic reticulum (SR) or not, the [Ca²⁺]_i transient induced by caffeine, that depletes the SR of Ca²⁺, was used as an indicator of Ca²⁺ content in the SR. The caffeine-induced [Ca²⁺]_i transient was significantly reduced by U50,488H at 20 μM. This effect of U50,488H on caffeine-induced [Ca²⁺]_i transient was significantly attenuated by 1 μM chelerythrine, indicating that the action of PKC involves mobilization of Ca²⁺ from the SR. When the increase in IP₃ production in response to κ-receptor stimulation with U50,488H in the ventricular myocyte was determined, the effect of U50,488H was the same in the presence and absence of staurosporine, suggesting that the effect of PKC activation subsequent to κ-receptor stimulation does not involve IP₃. The observations suggest that PKC may act directly at the SR.
4. In conclusion, the present study has provided evidence for the first time that PKC may be involved in the action of κ-receptor stimulation on Ca²⁺ in the SR and cyclic AMP production, both of which play an essential role in Ca²⁺ homeostasis in the heart.