The diagnostic utility of hypophosphatemia for differentiating generalized tonic-clonic seizures from syncope in dogs: A case control study.

Transient hypophosphatemia is often detected in humans following generalized tonic-clonic seizures (GTCS), and serum phosphorus concentration (sPi) serves as a marker to differentiate GTCS from syncope. The objective of this retrospective study was to assess the usefulness of hypophosphatemia as a diagnostic marker for GTCS in dogs. Eighty-seven and 26 client-owned dogs with GTCS or syncope, respectively, were enrolled. Dogs were included if the episode occurred ≤ 3 h from presentation, and if sPi and serum creatinine (sCr) were measured. Dogs were excluded if aged < 1 year or if sCr exceeded 176.8 µmol/L. There were no group differences in sCr. Hypophosphatemia (sPi ≤ 0.97 mmol/L) occurred in 28 dogs (32%) in the seizure group, and in no dogs in the syncope group. Median sPi was significantly (P < 0.001) lower in the seizure group (1 mmol/L, [range, 0.31-2.87 mmol/L]) compared to the syncope group (1.35 mmol/L [range, 0.97-2.71 mmol/L]). Furthermore, in dogs presented while seizing (n = 24/87; 28%) median sPi was significantly lower compared to those that were not (0.9 mmol/L [range, 0.3-1.74 mmol/L] vs. 1 mmol/L [range, 0.33-2.18 mmol/L], P = 0.050). ROC analysis of sPi as a marker of GTCS yielded an AUC of 0.757 (95% confidence interval 0.667-0.847), with an optimum cutoff point of 0.97 mmol/L, corresponding to specificity and sensitivity levels of 100% and 44%, respectively. In conclusion, sPi may, in certain cases, serve as an additional diagnostic tool to differentiate GTCS from syncope in dogs. Hypophosphatemia, especially with sPi < 0.97 mmol/L, may be useful in clinical practice to rule in GTCS.

Short-term heart rate variability in healthy dogs and dogs in various stages of degenerative mitral valve disease evaluated before pharmacotherapy.

Mitral valve disease (MVD) progression is associated with autonomic nervous system (ANS) imbalance. This study hypothesized that sympathetic and parasympathetic tones would be altered with MVD progression. ANS activity was assessed among different MVD classes in untreated dogs. This cross-sectional retrospective study included 29 healthy control dogs and 71 dogs with MVD divided according to American College of Internal Medicine (ACVIM) guidelines. Heart rate variability (HRV) analyses utilised time and frequency domains and were derived from 5 min, six-lead electrocardiogram recordings of sinus rhythm or respiratory sinus arrhythmia. While all time domain-related HRV parameters decreased with disease severity, only dogs in stage C exhibited significantly lower values (P < 0.05). High frequency (HF) band values decreased more than low frequency (LF) band values as disease severity increased (P < 0.05). The LF/HF ratio also progressively increased with MVD severity. A negative correlation was observed between HRV parameters and La/Ao ratio when the entire MVD case population was pooled (P < 0.05). Both sympathetic and parasympathetic tones were altered in dogs with MVD before clinical signs were observed and prior to the development of cardiomegaly. This is the first HRV study in untreated dogs with MVD. Investigating ANS imbalances preceding subclinical left-sided cardiomegaly in dogs with MVD should be considered in future age-matched, longitudinal studies to determine the potential benefits of early vagal tone augmentation in high-risk canine patients.

Obstructive right ventricular outflow tract myxosarcoma in an adult dog.

An 8-year-old female spayed German Shepherd cross was presented for acute onset of respiratory distress. Four days before presentation, the owner noticed a reduced appetite and reluctance to move. Clinical examination identified muffled lung sounds and a left base, diamond-shaped systolic murmur graded 4/6. Echocardiography identified pleural and pericardial effusion, ascites and a myxoid mass (39 mm/18.9 mm) obstructing the right ventricular outflow tract and interfering with the pulmonary valve function. Given the poor prognosis, the dog was euthanatised, and a postmortem examination was performed. Grossly, a mass with a heterogeneous appearance was identified below the pulmonary valve leaflets. Based on histopathological and immunohistochemical findings, a diagnosis of intracardiac myxosarcoma affecting the subvalvular region of the pulmonary artery was made. To the author's knowledge, this is the first report of right ventricle out flow tract myxosarcoma in the canine species.

Constant rate infusion vs. intermittent bolus administration of IV furosemide in 100 pets with acute left-sided congestive heart failure: A retrospective study.

The aim of this study was to determine whether the addition of constant rate infusion (CRI) to intermittent intravenous bolus (IVB) administration of furosemide resulted in an improvement in medical outcomes in dogs and cats with acute left-sided congestive heart failure (L-CHF). A total of 76 client-owned dogs and 24 client-owned cats admitted with acute L-CHF were retrospectively divided between an IVB group (43 dogs and 16 cats) and a CRI group (33 dogs and 8 cats). The median furosemide dose used in dogs in the CRI group (median 0.99mg/kg/h; range 0.025-3.73mg/kg/h) was lower than the dose used in dogs in the IVB group (median 1.19mg/kg/h; range 0.027-7.14mg/kg/h; P=0.008). Respiratory rates were lower in the IVB group (P=0.005) and the CRI group (P=0.039) compared to pre-treatment values. The overall short-term mortality was 15%. A trend of longer hospitalisation in the IVB group relative to the CRI group (P=0.07) was shown. Creatinine and total plasma protein concentrations increased more in the CRI group than in the IVB group, suggestive of a higher risk of dehydration and azotaemia. There may be safety profile differences between CRI and IVB, warranting a prospective study using a larger sample size.

Sleeping and resting respiratory rates in dogs and cats with medically-controlled left-sided congestive heart failure.

Sleeping and resting respiratory rates (SRR and RRR, respectively) are commonly used to monitor dogs and cats with left-sided cardiac disease and to identify animals with left-sided congestive heart failure (L-CHF). Dogs and cats with subclinical heart disease have SRRmean values <30 breaths/min. However, little is known about SRR and RRR in dogs and cats with CHF that is well controlled with medical therapy. In this study, SRR and RRR were measured by the owners of 51 dogs and 22 cats with stable, well-controlled CHF. Median canine SRRmean was 20 breaths/min (7-39 breaths/min); eight dogs were ≥25 breaths/min and one dog only was ≥30 breaths/min. Canine SRRmean was unrelated to pulmonary hypertension or diuretic dose. Median feline SRRmean was 20 breaths/min (13-31 breaths/min); four cats were ≥25 breaths/min and only one cat was ≥30 breaths/min. Feline SRRmean was unrelated to diuretic dose. SRR remained stable during collection in both species with little day-to-day variability. The median canine RRRmean was 24 breaths/min (12-44 breaths/min), 17 were ≥25 breaths/min, seven were ≥30 breaths/min, two were >40 breaths/min. Median feline RRRmean was 24 breaths/min (15-45 breaths/min); five cats had RRRmean ≥25 breaths/min; one had ≥30 breaths/min, and two had ≥40 breaths/min. These data suggest that most dogs and cats with CHF that is medically well-controlled and stable have SRRmean and RRRmean <30 breaths/min at home. Clinicians can use these data to help determine how best to control CHF in dogs and cats.

Murmur intensity in small-breed dogs with myxomatous mitral valve disease reflects disease severity.

OBJECTIVES: To determine whether murmur intensity in small-breed dogs with myxomatous mitral valve disease reflects clinical and echocardiographic disease severity. METHODS: Retrospective multi-investigator study. Records of adult dogs Ä20 kg with myxomatous mitral valve disease were examined. Murmur intensity and location were recorded and compared with echocardiographic variables and functional disease status. Murmur intensities in consecutive categories were compared for prevalences of congestive heart failure, pulmonary hypertension and cardiac remodelling. RESULTS: 578 dogs [107 with "soft" (30 Grade I/VI and 77 II/VI), 161 with "moderate" (Grade III/VI), 160 with "loud" (Grade IV/VI) and 150 with "thrilling" (Grade V/VI or VI/VI) murmurs] were studied. No dogs with soft murmurs had congestive heart failure, and 90% had no remodelling. However, 56% of dogs with "moderate", 29% of dogs with "loud" and 8% of dogs with "thrilling" murmurs and subclinical myxomatous mitral valve disease also had no remodelling. Probability of a dog having congestive heart failure or pulmonary hypertension increased with increasing murmur intensity. CLINICAL SIGNIFICANCE: A 4-level murmur grading scheme separated clinically meaningful outcomes in small-breed dogs with myxomatous mitral valve disease. Soft murmurs in small-breed dogs are strongly indicative of subclinical heart disease. Thrilling murmurs are associated with more severe disease. Other murmurs are less informative on an individual basis.

A loud right-apical systolic murmur is associated with the diagnosis of secondary pulmonary arterial hypertension: retrospective analysis of data from 201 consecutive client-owned dogs (2006-2007).

Canine pulmonary arterial hypertension (PAH) remains under-recognized and under-treated despite being prevalent. This retrospective study investigated whether selected historical and physical examination findings were associated with the diagnosis of canine PAH, defined as tricuspid regurgitation (TR) with a confirmed systolic pressure gradient ≥ 35 mm Hg. Two hundred and one client-owned dogs (PAH group, n=96; control group, n=105) were studied. Dogs in the control group had TR with a confirmed systolic gradient <35 mm Hg. All dogs underwent a complete physical examination and a complete echocardiographic assessment. A loud systolic right-apical murmur (RAM) was significantly associated with TR ≥ 35 mm Hg. The proportion of dogs with PAH significantly increased as the RAM grade increased, with odds ratios of 4.4-37.6 for Grades 3/6-5/6 (P=0.004 to <0.001), respectively. A stronger right-than-left apical-murmur had a positive predictive value (PPV) of 83% and was 96% specific for TR ≥ 35 mm Hg, and when combined with syncope, it had a PPV of 92% and was 92% specific. A Grade ≥ 4/6 RAM had a PPV of 85% and was 93% specific. Syncope with a Grade ≥ 4/6 RAM had a PPV of 94% and was 92% specific. Ascites combined with a Grade ≥ 4 or ≥ 5/6 RAM had a PPV of 100% and was 100% specific for TR ≥ 35 mm Hg. For each of these three murmur categories (Grades ≥ 4/6, ≥ 5/6, and a louder-right-than-left murmur), when detected with no concurrent ascites or syncope, the positive likelihood ratio varied from 4.6 to 6.4. A loud systolic RAM in dogs with degenerative valve disease is highly suggestive of concurrent PAH.

The occurrence and suspected mode of inheritance of congenital subaortic stenosis and tricuspid valve dysplasia in Dogue de Bordeaux dogs.

The Dogue de Bordeaux (DdB) breed has gone through several genetic 'bottle necks' and has a relatively small effective population size. Importing new stock into Israel has been limited, further narrowing the already restricted local gene-pool and increasing the chances of inherited defects. In 56 DdB dogs examined between 2003 and 2010, the authors sought to study the proportion congenital subaortic stenosis (SAS) and tricuspid valve dysplasia (TVD). The aim was also to identify a probable mode of inheritance (MOI) using segregation and pedigree analyses of genealogical data available from 13/21 DdB dogs diagnosed with these conditions between 2004 and 2007. Among all breeds in the country, TVD was highest in the DdB breed, which also displayed the second highest proportion of SAS. Echocardiographic measurements and selected physical examination findings from 26 normal DdB dogs, 18 DdB dogs with SAS, and 12 DdB dogs with TVD are reported. Based on pedigree and segregation analyses, the most probable MOI appeared to be autosomal recessive. Pedigree analyses helped to identify three ancestors that might have introduced these two congenital heart defects into the local DdB population. Excluding those three dogs and their progeny from future mating could therefore reduce the prevalence of these diseases in the DdB population in Israel. The unusual local breeding circumstances may offer a unique opportunity to identify associated SAS and TVD genes in the DdB, as well as in other dog breeds.

Sleeping respiratory rates in apparently healthy adult dogs.

Respiratory rate monitoring of cardiac patients is recommended by many cardiologists. However, little objective data exist about respiratory rates in apparently healthy dogs when collected in the home environment. We measured sleeping respiratory rates (SRR) in apparently healthy dogs and compared sleeping and resting respiratory rates (RRR) with a cross-sectional prospective study. Participants collected 12-14 one-minute SRR over a period ranging from 1 week to 2 months on 114 privately owned adult dogs. Selected participants simultaneously collected RRR. Mean within-dog average SRR (SRR(mean)) was 13breaths per minute (breaths/min). No dog had SRR(mean) >23 breaths/min; three dogs had instantaneous SRR measurements >30 breaths/min. Dogs had higher RRR(mean) (19 breaths/min) than SRR(mean) (15 breaths/min) (P<0.05). Canine SRR(mean) was unaffected by age, bodyweight or geographic location. Data acquisition was considered relatively simple by most participants. This study shows that apparently healthy adult dogs generally have SRR(mean) <30 breaths/min and rarely exceed this rate at any time.

Traumatic urothorax in a dog: a case report.

Pleural effusion caused by post-traumatic extravasation of urine from the abdominal cavity to the pleural cavity (urothorax) is an uncommon complication following traumatic injury. To the authors' knowledge, this is the first report of a case of traumatic urothorax in a dog presented with pleural and abdominal urine effusion. Combined urothorax and uroabdomen should be included in the differential-diagnosis list for dogs with recent trauma and a bicavitary effusion. The diagnosis can be confirmed by elevated creatinine concentrations in both effusates, compared to its serum concentration.

Cardiac arrhythmias and serum cardiac troponins in Vipera palaestinae envenomation in dogs.

BACKGROUND: Vipera palaestinae is responsible for most poisonous envenomations in people and animals in Israel. Cardiac arrhythmias were reported in a retrospective study of V. palaestinae envenomations in dogs. HYPOTHESIS: Cardiac arrhythmias in V. palaestinae-envenomed dogs are associated with myocardial injury reflected by increased serum concentrations of cardiac troponins (cTns). ANIMALS: Forty-eight client-owned dogs envenomed by V. palaestinae. METHODS: Blood sampling (serum biochemistry and cTns, CBC, and coagulation tests) and electrocardiography were performed periodically up to 72 hours postenvenomation. Cardiac rhythm strips were assessed blindly for the presence and type of arrhythmias. RESULTS: Serum cTn-T and cTn-I concentrations were increased in 25% (n = 12) and 65% (n = 31) of the dogs at least once during hospitalization, respectively. Arrhythmias were identified in 29% (n = 14) of the dogs. Dogs with increased cTn-T had a significantly higher occurrence of arrhythmias (58 versus 19%), and higher resting heart rate upon admission and within the following 24 hours. Dogs with increased serum cTn-T concentrations were hospitalized for a significantly (P= .001) longer period compared to those with normal serum cTn-T concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: Dogs envenomed by V. palaestinae appear to sustain some degree of myocardial injury, as reflected by increased serum cTn concentrations and by the occurrence of arrhythmias. The latter should alert clinicians to a potentially ongoing cardiac injury. An increase in cTn-T may be of clinical relevance and indicate a cardiac injury in V. palaestinae envenomations in dogs.

Cytotoxic T lymphocytes are activated following myocardial infarction and can recognize and kill healthy myocytes in vitro.

The damage of myocardial infarction (MI) is often progressive. A possible mechanism for subsequent myocardial damage and heart failure after MI is immune response against cardiac self-antigens. The purpose of our study was to test the hypothesis that cytotoxic T lymphocytes are activated following acute MI and may have a role in producing further myocardial damage. Rats were allocated into three experimental groups: acute MI, Sham MI and non-operated control. One, two and three weeks after surgery, lymphocytes were obtained from rat spleens and incubated with neonatal cardiac myocytes. Lymphocyte proliferation was assessed by a thymidine incorporation assay and calculated as proliferation index (PI). Myocyte destruction was measured by a crystal-violet staining assay and expressed as percentage of cell destruction. Proliferation index was significantly higher among lymphocytes obtained from MI animals (44. 3+/-5.8 and 44.9+/-5.1, at 2 and 3 weeks after MI, respectively) than sham MI (29.3+/-5.3, 27.1+/-4.7) (P<0.05) or control animals (17.1+/-2.5, 16.2+/-2.8) (P=0.03). Cytotoxic activity of the MI lymphocytes against the cultured cardiomyocytes was significantly higher 2 and 3 weeks after MI, (36.4+/-7.3%, 69.3+/-4.9%) compared to sham MI (17.9+/-3.14%, 36.6+/-5.3%) (P<0.001) and control animals respectively (13.3+/-5.4%, 17.4+/-6.1%) (P<0.001). The cytotoxic activity against healthy cardiomyocytes was myocyte-specific, induced by CD8 lymphocytes and major-histocompatibility complex (MHC) restricted. Cytotoxic T lymphocytes (CD8) are activated following MI and can recognize and kill normal cardiomyocytes in vitro. The newly described pathophysiological insights may provide novel oportunities to prevent death of non-ischemic cardiomyocytes and heart failure following myocardial infarction.

Parenteral administration of an activating monoclonal antibody to the alpha1beta1 integrin in dogs.

In mice, monoclonal antibody (mAb) to the alpha1 integrin abrogate gastro-intestinal damage during graft-versus-host-disease (GVHD), suggesting anti alpha1 mAb as candidates for treatment in humans as well. Our current data show that one such reagent, mAb 1B3.1, when immobilized to plastic wells via rabbit- anti murine (ram) immunoglobulin (Ig) induces a protein kinase-dependent spreading of activated human T cells. Furthermore, it significantly increases the proliferative response, and expression of interleukin-2 (IL-2) receptors (R) and CD69, of resting T cells, expressing minimal integrin on the cell surface, to sub-optimal stimulation by anti-CD3 mAb. We found, in addition, that mAb 1B3.1 a) immuno-precipitates alpha1beta1 integrins from cell-surface iodinated canine epithelial cells b) is highly reactive with canine T cells after their activation and c) inhibits adhesion of canine T cells to collagen IV. Despite the potential ability of the mAb to co-activate T cells in vitro, two dogs that received 4 injections of 0.5-0.3 mg/Kg of mAb 1B3.1 remained healthy, developing only marginal transient lymphopenia. Injection of 0.75mg/Kg in a third dog induced a more marked lymphopenia, and an additional dose of 1.0 mg/Kg 2 weeks later was followed by gastrointestinal hemorrhage. importantly, the lymphopenia was associated with a greater and more persistent decrease of CD8+ than of CD4+ T cells, leading to an increase in the CD4/CD8 ratio 24 hours after the injection. Thus, despite it's co-activating effects in vitro, administration of this mAb in vivo is feasible when appropriately dosed, and may have immuno-modulatory effects.

Electrocardiographic assessment of antianxiety medication in dogs and correlation with serum drug concentration.

OBJECTIVES: To determine effects of tricyclic antidepressants (TCA) on the ECG of dogs treated for behavioral conditions and to examine correlations between ECG findings and serum concentrations of these medications. DESIGN: Repeated-measures study. ANIMALS: 39 client-owned dogs with behavioral problems. PROCEDURE: Two groups of dogs with behavioral problems were evaluated. In group 1 (n = 20), ECG tracings were recorded before starting treatment with TCA and again after treatment for > or = 1 month. Dogs in group 2 were already on long-term maintenance amounts of antianxiety medication when ECG tracings were recorded and serum concentrations of medications were obtained. RESULTS: Significant differences were not detected for dogs in group 1 between ECG values measured before and after TCA administration. The ECG values for dogs in group 2 did not differ significantly from the mean of group-1 dogs before receiving medication or from the reference range used at our facility. Duration of the P wave had a significant positive correlation with serum concentrations of clomipramine but significant negative correlation with serum concentrations of amitriptyline. The QT interval corrected for heart rate had a significant negative correlation with serum concentrations of amitriptyline. CONCLUSIONS AND CLINICAL RELEVANCE: Amitriptyline and clomipramine administered at standard dosages apparently do not cause ECG abnormalities in healthy dogs with behavioral problems. These medications should be used cautiously in dogs with conduction abnormalities, and clinicians should periodically monitor ECG and use good clinical judgment to weigh risks and benefits of medications for the safety of each dog.

Basic fibroblast growth factor induces myocardial hypertrophy following acute infarction in rats.

Basic fibroblast growth factor (bFGF) is a potent mitogen which induces growth of collateral vessels in ischaemic and infarcted myocardium. The effect of systemically administered bFGF on left ventricular (LV) function, myocardial hypertrophy and LV remodelling following acute myocardial infarction (MI) have not yet been fully investigated. Thirty Sprague-Dawley male rats were randomized to receive bFGF (0.5 mg) or rat albumin intraperitoneally for 1 week, beginning immediately after the induction of MI. Five animals served as controls and did not undergo any operation. Animals were killed 6 weeks after surgery and the hearts were perfused and fixed at physiological pressure. Transverse cross-sections from infarcted areas were stained with antibodies against proliferating cell nuclear antigen (PCNA) and Masson-trichrome and analysed with a coloured-image analyser for LV area (mm2), LV cavity diameter (mm), infarcted area (%), and wall thickness (mm) in infarcted and non-infarcted regions. LV area was similar in MI rats and in controls (41.7 +/- 6.9 and 43.0 +/- 1.5 mm2, respectively) and was significantly larger in MI bFGF-treated (MI/bFGF) animals (47.6 +/- 7.1 mm2) (P = 0.023). LV cavity diameter was significantly larger in the MI group than in MI/bFGF and control animals (6.0 +/- 0.8, 4.9 +/- 1.4, and 4.4 +/- 0.8 mm, respectively, P = 0.018). Wall thickness in the non-infarcted region was significantly smaller in MI animals (1.4 +/- 0.3 mm) than in MI/bFGF animals (1.6 +/- 0.4 mm) and the control group (1.6 +/- 0.1 mm) (P = 0.015). The ratio between LV cavity diameter/non-MI wall thickness was higher in MI than in control and MI/bFGF groups (4.8 +/- 1.6, 2.7 +/- 0.6 and 3.3 +/- 1.8, respectively, P = 0.03). Proliferating endothelial cells were significantly more abundant in infarcted than in normal areas in both MI and MI/bFGF groups, but with no significant differences between the groups. Intraperitoneal administration of bFGF did not cause any untoward extracardiac effects. Thus, systemic bFGF administration following acute MI in rats prevents dilatation of the LV, induces hypertrophy of the non-infarcted myocardium and exerts no untoward effects on extracardiac organs.

Paresis and unusual electrocardiographic signs in a severely hypomagnesaemic, hypocalcaemic lactating bitch.

A severely hypocalcaemic, hypomagnesaemic lactating bitch exhibited clinical signs of pulmonary oedema, paresis, dementia, gastrointestinal ileus and urinary bladder atony. The total calcium, ionised calcium and magnesium levels were extremely low. The clinical picture was very different from the one typically encountered in canine lactation tetany, and instead resembled bovine postparturient paresis. Muscle tremors, rigidity and seizures were not part of the acute clinical picture, but rather atony, weakness and paresis. General muscle dysfunction probably resulted from the extremely low ionised calcium levels in combination with very low levels of magnesium and possibly potassium. Heart failure and atony of the urinary bladder and intestines were probably a result of the severe hypocalcaemia. The alteration in calcium to magnesium ratio may have depressed neuromuscular transmission, leading to paresis and atony. The unusual electrocardiogram possibly also resulted from abnormal magnesium and calcium cation levels.

Transcutaneous multielectrode basket catheter for endocardial mapping and ablation of ventricular tachycardia in the pig.

BACKGROUND: Endocardial mapping using standard electrode catheters is often technically limited in ventricular tachycardia and constitutes a major obstacle to successful ablation. We wished to examine the utility of a basket-shaped multielectrode mapping catheter (MMC) in the mapping and ablation of ventricular tachycardia. METHODS AND RESULTS: This study of sustained monomorphic ventricular tachycardia (SMVT) was conducted in two phases in the postinfarction pig model. In the first phase, the utility of the MMC in providing adequate localization of potential ablation site(s) of SMVT by different techniques (presystolic potentials, pace mapping, and concealed entrainment) was assessed in 21 pigs. In the second phase, ablation of induced SMVT was attempted in 10 pigs. Mapping of SMVT was performed after percutaneous introduction of the MMC to the LV. Comprehensive mapping was performed in 90 episodes of SMVT and required 2.0 to 25 seconds. Diastolic potentials were recorded during 86 episodes; good or identical pace maps (> or = 9 of 12 paced surface ECG leads identical to ventricular tachycardia surface ECG leads) were obtained in 25 of 31 maps, and entrainment was achieved during 28 of 42 SMVTs. In 10 pigs, 10 SMVTs were recorded at least twice and were considered for radiofrequency ablation. An 8-mm tip ablation catheter was advanced to potential ablation sites with a specially designed "homing" device, requiring a median time of 120 seconds. In these 10 pigs, either identical pace map (> or = 11 of 12, 6 SMVTs) or concealed entrainment (4 SMVTs) guided the ablation procedure. After ablation, 8 of 10 SMVTs were rendered noninducible, while 2 pigs died during energy application of degeneration of SMVT to ventricular fibrillation. CONCLUSIONS: The MMC allows rapid, comprehensive, and reliable endocardial mapping during SMVTs, which facilitates successful ablation in the porcine post-myocardial infarction model.

Echocardiographic imaging of a basket catheter for mapping and ablation of ventricular tachycardia in pigs.

Our objective was to assess the feasibility and efficacy of the recently described left ventricular simultaneous deployment of a new multi-electrode mapping catheter and a standard radio-frequency ablation catheter in pigs, with echocardiography monitoring and fluoroscopy guidance. Introduction and deployment of both catheters in five healthy anesthetized pigs were guided on-line by fluoroscopy and monitored with transthoracic echocardiography. Heart rate and femoral blood pressure were also continuously monitored. Both catheters were deployed for up to 5 hours. Three animals underwent three to five radio-frequency energy applications. Left ventricular dimensions obtained from long axis two-dimensional echocardiography imaging before and after basket-catheter deployment in the left ventricular cavity, were 3.9 +/- 0.3 versus 3.7 +/- 0.6 cm at end-diastole and 2.8 +/- 1.1 versus 2.6 +/- 0.8 cm at end-systole, respectively (mean +/- standard error of the mean, p > 0.05). Shortening fraction measured from long axis two-dimensional echocardiography images before and after catheter deployment was 28% +/- 10% versus 25% +/- 5%, respectively (mean +/- standard error of the mean, p > 0.05). Additional findings included the following: (1) good conformation of the multi-electrode mapping catheter to the left ventricular dimensions during diastole; (2) absence of catheter-induced aortic and/or mitral insufficiency, as well as left ventricular outflow tract obstruction; (3) absence of damage to mitral and aortic valves or to the left ventricular wall. Postmortem examination and hemodynamic measurements confirmed these findings and showed only minor subendocardial hemorrhages; (4) radio-frequency energy application produced intracavitary bubbles, which were demonstrable echocardiographically, enabling identification of the gross anatomic location of ablation sites. Echocardiography during simultaneous deployment of multi-electrode mapping catheter and radio-frequency ablation catheters enables estimation of mechanical interaction with the left ventricle and detects interaction with myocardial/valvular function. During radio-frequency energy application, bubble production may identify gross anatomic location of ablation.

Percutaneous multielectrode endocardial mapping and ablation of ventricular tachycardia in the swine model.

A basket shaped catheter carrying 64 electrodes was developed in the left ventricle (LV) of 53 pigs which had undergone induction of myocardial infarction. Pacing during sinus rhythm, or echocardiographic and hemodynamic measurements as well as pathological studies revealed no significant damage due to the basket catheter. Eighty one episodes of ventricular tachycardia (VT) were mapped and analyzed, requiring only several beats and less than 10 seconds to complete. We were able to successfully ablate ventricular tachycardias in four pigs.

Echocardiographic left ventricular remodeling and pseudohypertrophy as markers of hypovolemia. An experimental study on bleeding and volume repletion.

BACKGROUND: Monitoring intravascular volume during surgery, especially in major cardiovascular procedures is necessary for appropriate fluid restoration and the maintenance of an adequate cardiac output. In estimating preload, both standard hemodynamic and echocardiographic parameters have been limited. The purpose of this study was to further define the effects of induced hypovolemia on the echocardiographic parameters. In particular, we sought to show whether a decrease in echocardiographic left ventricular area and volume was associated with a significant increase in left ventricular wall thickness (left ventricular pseudohypertrophy) and with changes in LV function. In addition, we sought to investigate the effects of rapid restoration of blood volume on cardiac dimensions and function. METHODS AND RESULTS: Seven anesthetized pigs underwent systemic and right heart pressures and cardiac output measurements. Two-dimensional echocardiographic parasternal long- and short-axis views were obtained during graded bleeding by rapid withdrawal of blood from an arterial cannula, with increments of 5% each up to 30% of calculated blood volume. After completion of the bleeding, the entire amount of the blood withdrawn was retransfused within 4 to 5 minutes. Both hemodynamic and echocardiographic measurements were performed at baseline, immediately after the completion of each stage of bleeding and after blood restoration. Mean (+/- standard deviation) left ventricular wall thickness (mean of septal and posterior wall thickness) was 6.3 +/- 0.1 mm at baseline, 8.3 +/- 1.5 mm at peak bleeding, and 6.2 +/- 0.1 after restoration (p < 0.01). Left ventricular mass did not change during the experiment. Left ventricular end-diastolic volume was 62.8 +/- 20.3 ml at baseline, 37.5 +/- 12.4 ml at peak bleeding (p < 0.0001), and 65.9 +/- 16.7 ml after blood restoration (p < 0.001 compared with 30% bleeding). H/r ratio (posterior wall thickness divided by left ventricular radius) increased from 0.29 +/- 0.07 at baseline to 0.50 +/- 0.19 at peak bleeding returning to 0.26 +/- 0.04 after restoration. Left ventricular ejection fraction was 0.53 +/- 0.10 at baseline and 0.55 +/- 0.20 at peak bleeding (not significant), decreasing to 0.38 +/- 0.11 after blood restoration (p < 0.05 compared with 30% bleeding). End-diastolic volume correlated closely with right atrial pressure (r = -0.82), capillary wedge pressure (r = -0.78), and stroke volume (r = 0.74). Left ventricular ejection fraction inversely correlated with left ventricular end-diastolic volume (r = -0.48) and with end-systolic wall stress (r = -0.62). The changes in interventricular septal and posterior wall thickness were inversely related to left ventricular end-diastolic volume (r = -0.72 and -0.35, respectively). CONCLUSIONS: This study shows that transient concentric left ventricular remodeling (pseudohypertrophy), a phenomenon previously described in cardiac tamponade and during rapid atrial pacing is commonly seen during hypovolemia. This new sign may further enhance the echocardiographic estimation of left ventricular preload.