Congenital Subaortic Stenosis Research Articles

Incidence of Reoperation After Surgical Procedure for Left Ventricular Outflow Tract Obstruction in Children and Young Adults

BackgroundThe common causes of subaortic left ventricular outflow tract obstruction (LVOTO) are hypertrophic cardiomyopathy (HCM) and membranous/tunnel subaortic stenosis (SAS). Reoperation after corrective surgery may be due to recurrent disease, associated congenital defects, or complications of the initial procedure. This study compares the late outcomes of young patients with HCM and SAS. MethodsWe studied clinical, echocardiographic, and operative data of patients ≤21 years of age at the time of surgery for LVOTO between August 1963 and August 2018. We stratified patients into HCM (n = 152) and congenital SAS (n = 63) groups and compared survival and cumulative incidence of reoperation. ResultsAt initial repair, patients with HCM were older than patients with SAS (median [interquartile range] age, 15 [10-19] years vs 8 [5-13] years; P < .001), and patients with HCM were more symptomatic with dyspnea (P < .001), chest pain (P = .002), and presyncope/syncope (P = .005). Thirty-day mortality was 1.3% vs 0% for HCM and SAS groups. During a median follow-up of 13.1 years, survival was similar through the first 10 years; but during the second decade, patients with HCM had poorer survival (survival at 20 years, 80% vs 91% for patients with SAS; P = .007). Ten years after repair, reoperation for recurrent LVOTO was performed in 5% of patients with HCM vs 31% in those with SAS (P < .001). ConclusionsIn this surgical cohort, patients with HCM were more symptomatic preoperatively than those with SAS. Late survival of patients with SAS was superior to that of patients with HCM despite a greater need for reoperation.

Результаты хирургических вмешательств по поводу врожденного субаортального стеноза у детей различных возрастных групп

Результаты хирургических вмешательств по поводу врожденного субаортального стеноза у детей различных возрастных групп

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.

The Natural History of Congenital Subaortic Stenosis

Congenital subaortic stenosis (SAS) has a high recurrence rate after surgical correction. Aortic valve disease frequently coexists with SAS, being its occurrence and progression unpredictable. We aimed to assess predictors of SAS recurrence and aortic valve disease occurrence and progression. Retrospective analysis of 51 patients with SAS followed in a congenital heart disease clinic of a tertiary care hospital from July 1982 to October 2009. The mean age at SAS diagnosis was 15 years and 28 patients (54.9%) were men. Aortic regurgitation was present in 23 (45.1%) patients. Thirty-four (66.7%) patients were submitted to SAS surgical correction, six (17.6%) of them also with aortic valve repair/replacement. Eighteen (52.9%) patients had SAS recurrence and eight patients (23.5%) underwent reoperation. A shorter time from diagnosis to surgery (odds ratio [OR] 0.98 [95% confidence interval, CI 0.96-1.00]; P= 0.04) and a left ventricular outflow tract (LVOT) peak pressure gradient at diagnosis > 50 mm Hg (OR 2.63 [95% CI 1.52-4.53]; P= 0.05) were independent predictors of SAS recurrence. At the end of follow-up, 37 patients (72.5%) had some form of aortic valve disease and 24 patients (47.1%) had progression for or of the aortic valve disease. Higher LVOT peak pressure gradient at diagnosis (OR 1.10 [95% CI 1.01-1.21]; P= 0.05) and higher left ventricular mass (OR 1.04 [95% CI 1.01-1.07]; P= 0.014) were independent predictors of aortic valve disease. Predictors of aortic valve disease progression were not found. SAS recurrence occurred mainly in patients operated sooner and with a high LVOT peak pressure gradients, suggesting a more severe form of disease. A more turbulent systolic jet at LVOT was probably one of the main causes of aortic valve damage. Aortic valve disease progression occurred independently of surgery and SAS recurrence. All LVOT morphological anomalies should be detected and corrected in order to prevent SAS recurrence and aortic valve disease.

CULTURE NEGATIVE ENDOCARDITIS CAUSED BY BARTONELLA HENSELAE IN A CHILD WITH CONGENITAL HEART DISEASE

A 9-year-old white male with congenital aortic and subaortic stenosis palliated by the Ross-Konno procedure presented with culture-negative endocarditis. Serologic studies and polymerase chain reaction testing of resected homograft valvular tissue provided evidence of Bartonella henselae as the etiology. B. henselae can cause endocarditis in children, particularly those with underlying valvular disease. Serologic testing for B. henselae should be considered in children with culture-negative endocarditis.

Reoperation after relief of congenital subaortic stenosis☆

We read with interest the paper by Dodge-Khatami et al. [1] on risk factors for reoperation after relief of congenital subaortic stenosis. We compliment them on their extensive statistical analysis and would like to discuss their results as well as our own [2]. Preoperative left ventricular outflow tract (LVOT) gradients in their series ranged from 5 to 120 mmHg, which would lead us to question the need for operation with a preoperative gradient of only 5 mmHg (unless the stenosis was mild or combined with other lesions), their definition of significant postoperative gradients and their threshold for a reoperation. In our experience, and in those of others [3], a peak instantaneous gradient 30 mmHg is considered significant even in the presence of normal left ventricular (LV) function. Progression of LV hypertrophy, LV dysfunction and new aortic incompetence may necessitate operation regardless of the gradient. At a median follow-up of 2.6 years (range 0.3—7.5 years), the authors [1] report a reoperation rate of 19% (n = 11), of which 12 % (5/43) were in the simple group and 40% (6/15) were in the complex group. However, there is no detailed information about patients with immediate postoperative gradients, which may significantly correlate with long-term results [4]. Our experience with discreet subaortic membrane (SAM) consisted of 45 patients with a preoperative gradient of 50— 154 mmHg (86.5 33.2 mmHg); 19 of these had significant LV dysfunction. Transaortic resection of SAM was performed in all patients and was combined with the excision of a wedge shaped segment of septal muscle underlying the membrane. There were no early or late deaths and our follow-up ranged from 18 to 113 months (mean 67 4 months). Only four patients had significant gradients. In all these patients, the immediate postoperative gradients were 25, 20, 25 and 8 mmHg, respectively and progressed to 30—60 mmHg over a 2—5 year period. The actuarial freedom from significant gradients was 89.9 0.4% at 96 months. In one of these, the

Risk factors for reoperation after relief of congenital subaortic stenosis☆

Congenital subaortic stenosis entails a lesion spectrum, ranging from an isolated obstructive membrane, to complex tunnel narrowing of the left outflow associated with other cardiac defects. We review our experience with this anomaly, and analyze risk factors leading to restenosis requiring reoperation. From 1994 to 2006, 58 children (median age 4.3 years, range 7 days-13.7 years) underwent primary relief of subaortic stenosis. Patients were divided into simple lesions (n=43) or complex stenosis (n=15) associated with other major cardiac defects. Age, pre- and postoperative gradient over the left outflow, associated aortic or mitral valve insufficiency, chromosomal anomalies, arteria lusoria, and operative technique (membrane resection (22) vs associated myectomy (34) vs Konno (2)) were analyzed as risk factors for reoperation (Kaplan-Meier, Cox regression). There was no operative mortality. Median follow-up spanned 2.7 years (range 0.1-10), with one late death at 4 months. Reoperation was required for recurrent stenosis in 11 patients (19%) at 2.6 years (range 0.3-7.5) after initial surgery. Risk factors for reoperation included complex subaortic stenosis (p=0.003), younger age (p=0.012), postoperative residual gradient (p=0.019), and the presence of an arteria lusoria (p=0.014). For simple lesions, no variable achieved significance for stenosis recurrence. Surgical relief of congenital subaortic stenosis, even with complex defects, yields excellent results. Reoperation is not infrequent, and should be anticipated with younger age at operation, complex defects, residual postoperative gradient, and an arteria lusoria. Myectomy concomitant to membrane resection, even in simple lesions, does not provide enhanced freedom from reoperation, and should be tailored to anatomic findings.

Management of Symptoms in Hypertrophic Cardiomyopathy

In 1957, Brock1 made the distinction between congenital subaortic stenosis characterized by a fibrous ridge and “functional subvalvar stenosis” resulting from “muscular hypertrophy,” describing 3 patients with the latter. Brock initially attributed the hypertrophy and resultant outflow obstruction to systemic hypertension, a conclusion he withdrew in a 1959 publication.2 Between these 2 publications, Teare3 described asymmetrical septal hypertrophy in 8 autopsies (from a series of 16 000!). Remarkably, he identified myocyte disarray, proclivity for sudden death during exertion, and occurrence of stroke in association with atrial fibrillation as features of the disease. Quantitative definition of asymmetrical septal hypertrophy as septal to posterior wall thickness ratio ≥1.3 was introduced in 1961.4 The discovery that the left ventricular outflow tract (LVOT) gradient was created by systolic anterior motion (SAM) of the mitral valve was made from analysis of cineangiograms a year later.5 Soon thereafter, it was recognized that diverse patterns of hypertrophy existed. In the early 1970s, investigators came to realize that, even among patients with asymmetrical septal hypertrophy, obstruction to left ventricular (LV) outflow at rest was present in only a minority.6 The recognition that an impediment to LV inflow (eg, diastolic dysfunction) might be at least as important as any obstruction to outflow came with the observation that LV end-diastolic pressure (LVEDP) was elevated while LV end-diastolic volume (LVEDV) was normal or low in many patients with hypertrophic cardiomyopathy (HCM).7 The genetic basis of the disease was demonstrated in 1990.8 Half a century after the descriptions of Brock and Teare, HCM is now understood to be a disease characterized by idiopathic hypertrophy of the left (and occasionally right) ventricle. Although the disease is often inherited in an autosomal dominant pattern, there are many patients without any relatives who are known to have …

Long-term results of surgical repair in patients with congenital subaortic stenosis

The aim of the study was to analyze the long-term results of congenital subvalvar aortic stenosis (SAS) relief and the risk factors associated with recurrence and reoperations. Between January 1960 and March 2005, 190 patients underwent surgical correction for discrete (n=140) and tunnel (n=50) congenital subaortic stenosis. There were 115 male and 75 female patients ranging in age from 1 week to 36 years (mean age, 8.2+/-4.4 years). Preoperatively, 133 patients were in NYHA functional class I or II, 57 in class III or IV. There were several initial surgical procedures performed in patients with congenital subaortic stenosis: fibrous or fibromuscular subaortic resection, apical aortic conduit insertion, aortic valve replacement with mechanical valve, Ross and/or Konno procedure. There were 7 early (4%) and 10 late (5%) deaths. Actuarial survival including operative mortality of patients with discrete and tunnel SAS was 94% and 84% at 40 years (P=0.14), respectively. Within 7.1+/-6.2 years a recurrent peak aortic gradient >50 mmHg and moderate to severe aortic insufficiency were found in 50 patients (28%), all of whom had 104 reoperations. At late follow-up, ranging from 6 months to 42 years (mean 9.6+/-7.5 years), the left ventricle-aorta gradient was higher in patients with tunnel versus discrete obstruction (28+/-11 mmHg vs. 13+/-9 mmHg; P=0.01) with a 40-year poor freedom from reoperation (14% vs. 89%; P<0.001). Patients with tunnel SAS and complex multilevel left ventricular outflow tract obstruction required higher reoperation rates. Aortic valve replacement with pulmonary autograft (Ross procedure) performed at our institution resulted in low mortality and morbidity.

Surgical pathology of subaortic septal myectomy not associated with hypertrophic cardiomyopathy: A study of 98 cases (1996–2000)

Background: No series have described the surgical pathology of subaortic septal myectomy in patients with conditions other than hypertrophic cardiomyopathy (HCM). Methods: Medical records and microscopic slides were reviewed from 98 non-HCM patients undergoing septal myectomy at Mayo Clinic Rochester from 1996 to 2000. Concurrently, 204 other patients had myectomy for HCM. Results: The study group (65 women, 33 men) ranged in age from 1.5 to 92 years (mean, 61). Seventy underwent surgery for aortic stenosis (Group 1), 25 for congenital subaortic stenosis (Group 2) and 3 for other conditions (Group 3). Group 1 patients were older than Group 2 patients (72 vs. 26 years; P<.0001). Microscopic evaluation showed myocyte hypertrophy (97%), vacuolization (35%), left bundle branch tissue (26%) (33% in Group 1 vs. 8% in Group 2; P=.02) and disarray (19%); interstitial fibrosis (92%), inflammation (10%) and amyloidosis (7%, all prealbumin type, all Group 1, >80 years old); arterial thickening (18%) and dysplasia (12%), and dilated venules (6%); and endocardial fibrosis (74%) (64% in Group 1 vs. 100% in Group 2; P=.0001) and chronic inflammation (17%). Conclusions: Of 302 patients undergoing subaortic septal myectomy, 32% had conditions other than HCM. Myocyte disarray was present in 19% of patients without HCM (and was absent in 21% of HCM patients in a companion study). Thus, disarray alone cannot be used reliably to include or exclude a diagnosis of HCM in small surgical specimens. Because amyloid was found unexpectedly in seven elderly patients, we recommend routine amyloid staining on surgical myectomy tissue from patients ≥65 years old.

Problems in the Canine Left Ventricular Outflow Tract

Journal of Veterinary Internal MedicineVolume 15, Issue 5 p. 427-429 Open Access Problems in the Canine Left Ventricular Outflow Tract John D. Bonagura DVM, DACVIM, John D. Bonagura DVM, DACVIM Department of Veterinary Clinical Sciences College of Veterinary Medicine Ohio State University Columbus, OH 43210 e-mail: [email protected]Search for more papers by this author John D. Bonagura DVM, DACVIM, John D. Bonagura DVM, DACVIM Department of Veterinary Clinical Sciences College of Veterinary Medicine Ohio State University Columbus, OH 43210 e-mail: [email protected]Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2001.tb01570.xCitations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Buchanan JW. Prevalence of cardiovascular disorders. In: PR Fox, DD Sisson, NS Moise, eds. Textbook of Canine and Feline Cardiology. Philadelphia , PA : WB Saunders; 1999: 457– 470. 2 Kienle RD, Thomas WP, Pion PD. The natural clinical history of canine congenital subaortic stenosis. J Vet Intern Med 1994; 8: 423– 431. 3 Pyle RL, Patterson DF, Chacko S. The genetics and pathology of discrete subaortic stenosis in the Newfoundland dog. Am Heart J 1976; 92: 324– 334. 4 Bussadori C, Amberger C, Le Bobinnec G, Lombard CW. Guidelines for the echocardiographic studies of suspected subaortic and pul-monic stenosis. J Vet Cardiol 2000; 2: 17. 5 Sisson DD, Thomas WP, Bonagura JD. Congenital heart disease. In: SJ Ettinger, EC Feldman, eds. Textbook of Veterinary Internal Medicine, 5th ed. Philadelphia , PA : WB Saunders; 2000: 737– 787. 6 Lehmkuhl LB, Bonagura JD. Comparison of catheterization and Doppler-derived pressure gradients in a canine model of subaortic stenosis. J Am Soc Echocardiogr 1995; 8: 611– 620. 7 Weyman AE, Griffin BP Left ventricular outflow tract: The aortic valve, aorta, and subvalvular outflow tract. In: AE Weyman, ed. Principles and Practice of Echocardiography, 2nd ed. Philadelphia , PA : Lea & Febiger; 1994: 498– 574. 8 Bélanger MC, DiFruscia R, Dumesnil JG, Pibarot P. Usefulness of the indexed effective orifice area in the assessment of subaortic stenosis in the dog. J Vet Intern Med 2001; 15: 430– 437. 9 Orton EC, Herndon GD, Boon JA, et al. Influence of open surgical correction on intermediate-term outcome in dogs with subvalvular aortic stenosis: 44 cases (1991–1998). J Am Vet Med Assoc 2000; 216: 364– 367. 10 Lehmkuhl LB, Bonagura JD. Comparison of transducer placement sites for Doppler echocardiography in dogs with subaortic stenosis. Am J Vet Res 1994; 55: 192– 198. 11 Brown DJ, Knight DH, King RR. Use of pulsed-wave Doppler echocardiography to determine aortic and pulmonary velocity and flow variables in clinically normal dogs. Am J Vet Res 1991; 52: 543– 550. Citing Literature Volume15, Issue5September 2001Pages 427-429 ReferencesRelatedInformation

Minimally invasive resection of congenital subaortic stenosis

Fifteen consecutive patients with membranous subaortic stenosis underwent resection by a minimal-access approach through a partial upper sternotomy using a cardioscope. There were no operative deaths and no postoperative complications. Twelve patients (80%) were extubated in the operating room. The mean hospital stay was 3.1 days, and 3 patients (20%) needed blood products. Our experience demonstrates that this modified approach is a safe and effective surgical option for resection of subaortic stenosis.

Congenital subaortic stenosis by accessory mitral valve tissue, recognition and management

Accessory mitral valve tissue as the single cause for left ventricular outflow tract obstruction is a very rare cardiac malformation in normally connected hearts. We report a case in which this condition was present as single cause for left ventricular outflow tract obstruction. The surgical technique is described and a review of the literature presented.

The natural clinical history of canine congenital subaortic stenosis.

The demographics and natural clinical history of canine congenital subaortic stenosis (SAS) were evaluated by retrospective analysis of 195 confirmed cases (1967 to 1991), 96 of which were untreated and available for follow-up evaluation. Of these, 58 dogs had left ventricular outflow systolic pressure gradients available for assessment of severity. All 195 dogs were used for demographic analysis. Breeds found to be at increased relative risk included the Newfoundland (odds ratio, 88.1; P < .001), Rottweiler (odds ratio, 19.3; P < .001), Boxer (odds ratio, 8.6; P < .001), and Golden Retriever (odds ratio, 5.5; P < .001). Dogs with mild gradients (16 to 35 mm Hg) and those that developed infective endocarditis or left heart failure were diagnosed at older ages than those with moderate (36 to 80 mm Hg) and severe (> 80 mm Hg) gradients. Of 96 untreated dogs, 32 (33.3%) had signs of illness varying from fatigue to syncope; 11 dogs (11.3%) developed infective endocarditis or left heart failure. Exercise intolerance or fatigue was reported in 22 dogs, syncope in 11 dogs, and respiratory signs (cough, dyspnea, tachypnea) in 9 dogs. In addition, 21 dogs (21.9%) died suddenly. Sudden death occurred mainly in the first 3 years of life, primarily but not exclusively, in dogs with severe obstructions (gradient, > 80 mm Hg; odds ratio, 16.0; P < .001). Infective endocarditis (6.3%) and left heart failure (7.3%) tended to occur later in life and in dogs with mild to moderate obstructions.(ABSTRACT TRUNCATED AT 250 WORDS)

Transaortic Resection of the Subaortic Membrane: Treatment for Subvalvular Aortic Stenosis

In an attempt to better understand congenital subaortic stenosis, we reviewed 19 consecutive pediatric patients undergoing surgery for this problem between 1973 and 1984. Preoperative cardiac catheterization demonstrated subvalvular stenosis in all patients and associated anomalies in 11 patients. All patients underwent transaortic resection of the subaortic membrane. Five patients underwent concurrent additional cardiac procedures. An 8-month-old infant with multiple cardiac anomalies was the only operative mortality. Follow-up extended to 16 years, with a mean of 6.9 years. In five symptomatic patients, cardiac catheterization revealed a mean systolic pressure gradient of 33.0 +/- 31.94 mm Hg 24.7 months (mean) after surgery. Two of these patients (11.1 percent of survivors) required reoperation. Twelve of the remaining 13 asymptomatic patients underwent echocardiographic follow-up, and 4 were found to have recurrent stenosis with 1 requiring surgery (5.6 percent of survivors). Our experience shows that transaortic resection of the subaortic membrane is an acceptable treatment for subvalvular aortic stenosis, but is associated with a high incidence of recurrence requiring reoperation (3 of 18 or 16.7 percent). Consequently, it is reasonable to consider the role of alternative therapies which may help prevent recurrence in selected cases.

Balloon dilation of congenital subaortic stenosis in the dog.

Balloon dilation during cardiac catheterization was evaluated for the treatment of congenital subaortic stenosis (SAS) in nine dogs. Under general anesthesia, bilateral cardiac catheterization was performed through the right jugular vein and carotid artery. Thermodilution cardiac output, and left ventricular and aortic root pressures and angiograms were obtained before and after balloon dilation. Balloons measuring 18-20 mm in diameter and 30-40 mm in length were positioned across the stenosis and three inflations 4-5 minutes apart were performed. There was no significant change in cardiac output, aortic pressure, or degree of aortic regurgitation after balloon dilation. For the entire group balloon dilation resulted in significant decreases in left ventricular systolic pressure (-61.2 +/- 37.2 mm Hg [mean change +/- SD], range -14 to -123), mean systolic pressure gradient (-39.6 +/- 24.4 mm Hg, range -8.4 to -72.2), and peak systolic pressure gradient (-64.3 +/- 46.5 mm Hg, range -17 to -143). Calculated left ventricular outflow cross-sectional area increased significantly (+.4 +/- .5 cm2, range -.06 to + 1.30). Clinical signs improved in the five symptomatic dogs. Individual hemodynamic responses varied widely, but the magnitude of improvement correlated with the severity of obstruction. Three dogs showed a decrease of 60% or greater (> or = 100 mm Hg), and six dogs showed a decrease of 25-50% (17-71 mm Hg) in peak systolic gradient after balloon dilation. Complications were frequent but most were transient and manageable. These preliminary results suggest that balloon dilation can acutely decrease outflow resistance in dogs with SAS and may be effective therapy for some affected dogs.

Spontaneous and induced arterial disease in the dog: pathology and pathogenesis.

The spontaneous arterial diseases of the dog relevant to safety assessment studies of drugs are the extramural coronary arteritis of Hartman, intramural coronary arteriosclerosis (with amyloid deposition) occurring in older dogs with cardiac disability, intramural arteriosclerosis without amyloid deposition in the left ventricle of dogs with congenital subaortic stenosis or in the right ventricle in dogs with severe pulmonic stenosis, and necrotizing polyarteritis (nodosa). Experimentally induced lesions include right atrial necrosis and arteritis produced by minoxidil and theobromine, extramural coronary arteritis produced by positive inotropic/vasodilator drugs, intramural coronary arteriosclerosis associated with decreased peripheral resistance and tachycardia induced by hypotensive drugs (including antihypertensive and positive inotropic/vasodilator agents), and intramural arteriosclerosis associated with rapid ventricular pacing. The pathogenesis of none of these lesions is known. The left ventricular subendocardial and papillary muscle intramural coronary arterial lesions are associated with hyperdynamic activity and, in the case of drugs and subaortic stenosis, the possibility of lowered perfusion pressure and tachycardia. This has led to the supposition that these are ischemic lesions, but the evidence available either does not support or refutes that conclusion since subendocardial coronary flow and perfusion pressure are adequate with pacing tachycardia and in toxicity trials. Necrotizing polyarteritis appears to be an immune mediated disease that may appear in genetically prone beagles when they are placed under the stresses of experimental manipulation and/or a new environment. Since the right atrial minoxidil lesion can also be produced by theobromine in dogs and minoxidil can cause a left atrial lesion in swine, it is neither species nor drug specific. Its cause, however, escapes us. There appears to be little in common between the extramural coronary artery Hartman lesion and that caused by positive inotropic/vasodilator drugs. Left ventricular subendocardial and papillary muscle intramural coronary arterial lesions induced by ventricular pacing at 250 beats/min for 2 months are generally similar to those seen in toxicity trials with peripheral vasodilator drugs that induce tachycardia in electrocardiograms exceeding 200 beats/min, although in acute pacing experiments subendocardial perfusion is adequate at these heart rates. Coronary artery autoregulation may be compromised or so destabilized by the drugs that episodes of underperfusion can account for these lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Regional myocardial blood flow in left ventricular hypertrophy: An experimental investigation in Newfoundland dogs with congenital subaortic stenosis

To test the hypothesis that left ventricular hypertrophy (LVH) may predispose the subendocardium to ischemia, we studied regional myocardial blood flow in dogs with the fibrous ring form of subvalvular aortic stenosis and concentric LVH. Radioactive microspheres, 9 +/- 1 mu in diameter, were used. Eleven dogs with LVH (left ventricular body weight ratio of 6.35 +/- 0.46 gm/kg [mean +/- SEM] and peak left ventricular outflow gradient of 51 +/- 7 mm Hg) were compared to 12 normal dogs (left ventricular/body weight ratio of 3.41 +/- 0.12 gm/kg and peak left ventricular outflow gradient of 6 +/- 3 mm Hg). The two groups of dogs were subjected to comparable experimental interventions including (1) tachycardia produced by atrial pacing (221 +/- 4 beats/min), (2) ascending aortic constriction producing systolic hypertension (212 +/- 5 mm Hg), and (3) creation of an aortic-right atrial fistula lowering diastolic blood pressure (38 +/- 3 mm Hg). Basal regional myocardial blood flow was distributed similarly for LVH and normal dogs (endocardial/epicardial ratio = 0.90 +/- 0.05 and 0.94 +/- 0.03, respectively). During experimental interventions, regional blood flow remained equal to all myocardial layers in normal dogs; however, the endocardial/epicardial ratio diminished in LVH dogs during atrial tachycardia to 0.61 +/- 0.08, during systolic hypertension to 0.68 +/- 0.06, and during diastolic hypotension to 0.50 +/- 0.09. When the diastolic/systolic pressure time index ratio (DPTI/SPTI) was less than 0.8, subendocardial ischemia occurred in dogs with LVH (endocardial/epicardial ratio = 0.66 +/- 0.04) but not in normal dogs (endocardial/epicardial ratio = 0.92 +/- 0.03) (p less than 0.0001). Animals with infracoronary obstruction and LVH demonstrate greater susceptibility to development of subendocardial ischemia for identical hemodynamic interventions than do normal animals.

The ultrastructure of sarcomeres in hypertrophied canine myocardium in spontaneous subaortic stenosis.

Ultrastructural alterations of sarcomeric structure were found in canine congenital subaortic stenosis leading to cardiac hypertrophy.

Left circumflex coronary artery hemodynamics in conscious dogs with congenital subaortic stenosis.

Coronary arterial hemodynamics were studied in three conscious dogs with congenital fibrous ring-type subaortic stenosis. Flow characteristics were recorded with electromagnetic flow transducers chronically implanted on the circumflex branch of the left coronary artery. Circumflex resting flow (ml/min 100 g -1 myocardium) was below that previously found in normal dogs studied by the same methods. Phasic coronary flow patterns at rest were abnormal, being characterized by reversed flow throughout most of ventricular systole. The mean reactive hyperemic response after 10 seconds of mechanical occlusion was comparable to that in normal dogs despite the essential absence of systolic forward flow. In one dog, moderate treadmill exercise substantially increased total circumflex flow despite a large increase in reversed circumflex flow.