A vortical hot tower route to tropical cyclogenesis Nicholls, M. E. ABSTRACT A nonhydrostatic cloud model is used to examine the thermomechanics of tropical cyclogenesis under realistic meteorological conditions. Observations motivate the focus on the problem of how a midtropospheric cyclonic vortex, a frequent by-product of mesoscale convective systems during summertime conditions over tropical oceans, may be transformed into a surface-concentrated (warm core) tropical depression. As a first step, the vortex transformation is studied in the absence of vertical wind shear or zonal flow.Within the cyclonic vorticity-rich environment of the mesoscale convective vortex (MCV) embryo, the simulations demonstrate that small-scale cumulonimbus towers possessing intense cyclonic vorticity in their cores [vortical hot towers (VHTs)] emerge as the preferred coherent structures. The VHTs acquire their vertical vorticity through a combination of tilting of MCV horizontal vorticity and stretching of MCV and VHT-generated vertical vorticity. Horizontally localized and exhibiting convective lifetimes on the order of 1 h, VHTs overcome the generally adverse effects of downdrafts by consuming convective available potential energy in their local environment, humidifying the middle and upper troposphere, and undergoing diabatic vortex merger with neighboring towers.During metamorphosis, the VHTs vortically prime the mesoscale environment and collectively mimic a quasi-steady diabatic heating rate within the MCV embryo. A quasi-balanced toroidal (transverse) circulation develops on the system scale that converges cyclonic vorticity of the initial MCV and small-scale vorticity anomalies generated by subsequent tower activity. The VHTs are found to accelerate the spinup of near-surface mean tangential winds relative to an approximate axisymmetric model that excises the VHTs. This upscale growth mechanism appears capable of generating a tropical depression vortex on time scales on the order of 1-2 days, for reasonable parameter choices.Further tests of the VHT paradigm are advocated through diagnoses of operational weather prediction models, higher resolution simulations of the current configuration, examination of disruption scenarios for incipient vortices, and a meteorological field experiment.

BackgroundPimobendan is effective in treatment of dogs with congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD). Its effect on dogs before the onset of CHF is unknown.Hypothesis/ObjectivesAdministration of pimobendan (0.4–0.6 mg/kg/d in divided doses) to dogs with increased heart size secondary to preclinical MMVD, not receiving other cardiovascular medications, will delay the onset of signs of CHF, cardiac‐related death, or euthanasia.Animals360 client‐owned dogs with MMVD with left atrial‐to‐aortic ratio ≥1.6, normalized left ventricular internal diameter in diastole ≥1.7, and vertebral heart sum >10.5.MethodsProspective, randomized, placebo‐controlled, blinded, multicenter clinical trial. Primary outcome variable was time to a composite of the onset of CHF, cardiac‐related death, or euthanasia.ResultsMedian time to primary endpoint was 1228 days (95% CI: 856–NA) in the pimobendan group and 766 days (95% CI: 667–875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47–0.87) compared with the placebo group. The benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952–NA) in the pimobendan group and 902 days (95% CI: 747–1061) in the placebo group) (P = .012).Conclusions and Clinical ImportanceAdministration of pimobendan to dogs with MMVD and echocardiographic and radiographic evidence of cardiomegaly results in prolongation of preclinical period and is safe and well tolerated. Prolongation of preclinical period by approximately 15 months represents substantial clinical benefit.

BackgroundPublished information regarding survival and long‐term cardiac remodeling after patent ductus arteriosus (PDA) closure in dogs is limited.ObjectivesTo report outcome and identify prognostic variables in dogs with PDA, and to identify risk factors for persistent remodeling in dogs with a minimum of 12 months of follow‐up after closure.AnimalsFive hundred and twenty client‐owned dogs.MethodsRetrospective review of medical records of 520 dogs with PDA. Outcome was determined by contacting owners and veterinarians. Dogs with PDA closure and ≥ 12 months of follow‐up were asked to return for a re‐evaluation.ResultsIn multivariable analysis of 506 dogs not euthanized at the time of diagnosis, not having a PDA closure procedure negatively affected survival (HzR = 16.9, P < .001). In 444 dogs undergoing successful PDA closure, clinical signs at presentation (HzR = 17, P = .02), concurrent congenital heart disease (HD) (HzR = 4.8, P = .038), and severe mitral regurgitation (MR) documented within 24 hours of closure (HzR = 4.5, P = .028) negatively affected survival. Seventy‐one dogs with ≥ 12 months follow‐up demonstrated a significant reduction in radiographic and echocardiographic measures of heart size (P = 0) and increased incidence of acquired HD (P = .001) at re‐evaluation. Dogs with increased left ventricular size and low fractional shortening at baseline were more likely to have persistent remodeling at re‐evaluation.Conclusions and Clinical ImportancePatent ductus arteriosus closure confers important survival benefits and results in long‐term reverse remodeling in most dogs. Clinical signs at presentation, concurrent congenital HD, and severe MR negatively affect survival. Increased left ventricular systolic dimensions and systolic dysfunction at baseline correlated significantly with persistent remodeling.

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Chylothorax is a devastating disease, and the success rates from either medical or surgical management are less than satisfactory. In some animals with chylothorax, a thickening of the pericardium occurs that is associated with chronic irritation induced by chyle. We hypothesized that pericardial thickening would lead to increased right-sided venous pressures and that abnormal venous pressures would act to impede the drainage of chyle via lymphaticovenous communications after thoracic duct (TD) ligation. We also hypothesized that serosanguineous effusions that occurred after TD ligation could effectively be treated or prevented by pericardectomy in affected animals. TD ligation plus pericardectomy was performed in 17 animals, and pericardectomy alone was performed in an additional 3 animals that presented during a 5.5-year period to the Texas A&M University (College Station, TX). Nineteen animals presented for an evaluation of idiopathic chylothorax (9 dogs and 10 cats), and 1 dog presented for serosanguineous pleural fluid after TD ligation that had been performed elsewhere. Echocardiography was normal in all animals, except for a subjectively thickened pericardium in 7 cats and 6 dogs. Clinical signs of pleural fluid accumulation resolved in 10 of 10 dogs and in 8 of 10 cats after surgery. The overall success rate for the surgical treatment of chylothorax (ie, the resolution of pleural fluid accumulation) in this study was 90% (100% in dogs and 80% in cats). These data suggest that TD ligation in conjunction with pericardectomy has a favorable outcome in animals with idiopathic chylothorax.