Presence Of Right Ventricular Hypertrophy Research Articles

Do athletic ECG changes predict athletic performance in Gurkha recruits?

IntroductionECG changes are associated with regular long-term intensive exercise due to electrical manifestations of increased vagal tone, increased ventricular wall thickness and enlarged chamber size. The aim of this study...

Assessing right ventricular deformation in hypertrophic cardiomyopathy patients with preserved right ventricular ejection fraction: a 3.0-T cardiovascular magnetic resonance study

To assess the global and regional right ventricular (RV) deformation in hypertrophic cardiomyopathy (HCM) patients with preserved right ventricular ejection fraction (RVEF) using 3.0-T cardiovascular magnetic resonance tissue tracking (CMR-TT). Eighty-two HCM patients and 32 age- and sex-matched healthy controls were enrolled. HCM patients were divided into groups depending on the presence or absence of right ventricular hypertrophy (RVH), RV late gadolinium enhancement (RV-LGE), and left ventricular outflow tract obstruction (LVOTO), respectively. The RV global and apical longitudinal peak strain (LPS) in HCM patients with RVH were significantly lower than that in HCM patients without RVH and controls (P < 0.05). The global, apical and mid-ventricular LPS in HCM patients with RV-LGE were significantly lower than that in HCM patients without RV-LGE and controls (P < 0.05). Lower LPS was demonstrated in HCM patients without RV-LGE compared with controls in apical and mid-ventricular levels (P < 0.05). No significant difference was found regarding global and regional LPS in HCM patients with LVOTO compared without LVOTO (all P > 0.05). CMR-TT was able to detect subclinical RV myocardial deformation prior to RVEF impairment, which was more severe in the presence of RVH and RV-LGE.

A 12-Lead ECG-Based System With Physiological Parameters and Machine Learning to Identify Right Ventricular Hypertrophy in Young Adults.

Objective: The presence of right ventricular hypertrophy (RVH) accounts for approximately 5-10% in young adults. The sensitivity estimated by commonly used 12-lead electrocardiographic (ECG) criteria for identifying the presence of RVH is under 20% in the general population. The aim of this study is to develop a 12-lead ECG system with the related information of age, body height and body weight via machine learning to increase the sensitivity and the precision for detecting RVH. Method: In a sample of 1,701 males, aged 17–45 years, support vector machine is used for the training of 31 parameters including age, body height and body weight in addition to 28 ECG data such as axes, intervals and wave voltages as the inputs to link the output RVH. The RVH is defined on the echocardiographic finding for young males as right ventricular anterior wall thickness > 5.5 mm. Results: On the system goal for increasing sensitivity, the specificity is controlled around 70-75% and all data tested in the proposed method show competent sensitivity up to 70.3%. The values of area under curve of receiver operating characteristic curve and precision-recall curve using the proposed method are 0.780 and 0.285, respectively, which are better than 0.518 and 0.112 using the Sokolow-Lyon voltage criterion, respectively, for detecting unspecific RVH. Conclusion: We present a method using simple physiological parameters with ECG data to effectively identify more than 70% of the RVH among young adults. Clinical Impact: This system provides a fast, precise and feasible diagnosis tool to screen RVH.

Selective Sexual Dimorphisms in Musculoskeletal and Cardiopulmonary Pathologic Manifestations and Mortality Incidence in the Tumor Necrosis Factor-Transgenic Mouse Model of Rheumatoid Arthritis.

To examine and quantify the sexual dimorphism in pathologic features manifested in the musculoskeletal and cardiopulmonary systems and incidence of mortality in the tumor necrosis factor-transgenic (TNF-Tg; Tg3647 strain) mouse model of inflammatory erosive arthritis. Kaplan-Meier survival estimates were determined in male and female Tg3647 mice and sex-matched wild-type (WT) littermate mice. Longitudinal and cross-sectional pathologic outcomes in the musculoskeletal and cardiopulmonary systems were assessed via ultrasound, micro-computed tomography, grip strength measurements, histologic and serologic analyses, flow cytometry, and skeletal muscle physiologic measures. Compared to male Tg3647 mice (n = 30), female Tg3647 mice (n = 34) had significantly shorter lifespans (P < 0.001) and exhibited the following pathologic features (n = 4-6 per group; P < 0.05 versus male Tg3647 littermates): gross deficits in body mass and muscle weight, early-onset inflammatory arthritis with severity of end-stage arthritis that was as severe as that seen in male transgenic mice, and early onset and increased severity of inflammatory interstitial lung disease (ILD). Histologically, the ILD observed in Tg3647 mice was characterized by inflammatory cell accumulation and pulmonary arteriole thickening, which was concomitant with the presence of right ventricular hypertrophy, a feature that was also more severe in the female compared to male Tg3647 mice (P < 0.05). No sexual dimorphisms in TNF-induced deficient grip strength, axial skeletal growth, or bone loss were found. Globally, the extent of the pathologic changes observed in female Tg3647 mice was greater than that observed in male Tg3647 mice when each group was compared to their sex-matched WT littermates. These findings indicate that TNF selectively drives the early onset of arthritis and progression of pathologic changes in the cardiopulmonary system in female Tg3647 mice. These results in the Tg3647 mouse identify it as a suitable model to better understand the mechanisms underlying sexual dimorphism and cardiopulmonary disease in the setting of inflammatory arthritis and other connective tissue diseases.

Role of catestatin in 2K1C-induced renal hypertension in rats and the underlying mechanism

To investigate the roles of catestatin (CST) in 2-kidney-1 clip (2K1C)-induced renal hypertension in rats, and to explore the underlying mechanism. Thirty six male SD rats were randomly divided into Sham group (n=15) and Model group(n=21).The model group was performed by 2K1C operation. For 2K1C operation, the left renal arteries were narrowed by cotton thread. The Sham group was treated with the same condition as the 2K1C group except the renal artery was narrowed. Tail-cuff systemic blood pressure of rats was measured before and every weeks after 2K1C operation. Six weeks after 2K1C operation, a carotid artery catheter was inserted to measure blood pressure of rats under anesthesia. Then, the model group was randomly subdivided into 2K1C group (n=15) and 2K1C+CST group (n=6). The rats of 2K1C+CST group were intravenous given CST (80 μg/100 g) and the rats of Sham or 2K1C group were given normal saline. All rats were sacrificed after blood pressure was measured and blood was collected. Then, the left ventricular plus interventricular septum weight (LV+S) was weighted and the ratio of (LV+S)/body weight(BW) was calculated as the index of left ventricular hypertrophy. Norepinephrine (NE) contents in plasma were determined by high performance liquid chromatography(HPLC) and CST contents in plasma by ELISA. The nitrite/nitrate contents in the left ventricular tissue and plasma were measured by nitrate reduction method to represent nitric oxide (NO)contents.Expression levels of CST in the left ventricle, kidney, medulla oblongata and adrenal gland,as well as eNOS and iNOS, were tested by Western blot. ①The 2K1C group had higher tail-artery blood pressure(P<0.01) and were more marked presence of right ventricular hypertrophy than those of sham group (P<0.01). Compared with Sham group, plasma CST content in 2K1C group was decreased by 226% (P<0.01), while plasma NE content in 2K1C group was increased by 246% (P<0.01), expression levels of chromograminA(Chga) in medulla oblongata of 2K1C group were increased by 108%, in leftventricle and kidneywere decreased by 60% and 30%, respectively (P<0.05).the content of NO in left ventricular and plasmawere increased by 46% and 24% respectively. ②The carotid arterial blood pressure of 2K1C group markedly reduced after administration of CST.③Compared with 2K1C group, the content of NO in left ventricul and plasma of 2K1C+CST group were increased by 35% and 19% respectively(P<0.05). The expression of eNOS in left ventricular of 2K1C+CST group were also obviously increased. The CST expression of 2K1C-induced renal hypertension rats is reduced and the effects of exogenous CST lowering their blood pressure may be related to NO/NOS system.Therefore, we speculate CST could contribute to the pathogenesis and progression of renal hypertension.

Effects of the association of diabetes and pulmonary emphysema on cardiac structure and function in rats.

Chronic obstructive pulmonary disease is often associated with chronic comorbid conditions of cardiovascular disease, diabetes mellitus and hypertension. This study aimed to investigate the effects of the association of diabetes and pulmonary emphysema on cardiac structure and function in rats. Wistar rats were divided into control non-diabetic instilled with saline (CS) or elastase (CE), diabetic instilled with saline (DS) or elastase (DE), DE treated with insulin (DEI) groups and echocardiographic measurements, morphometric analyses of the heart and lungs, and survival analysis conducted 50 days after instillation. Diabetes mellitus was induced [alloxan, 42 mg/kg, intravenously (iv)] 10 days before the induction of emphysema (elastase, 0.25 IU/100 g). Rats were treated with NPH insulin (4 IU before elastase plus 2 IU/day, 50 days). Both CE and DE exhibited similar increases in mean alveolar diameter, which are positively correlated with increases in right ventricular (RV) wall thickness (P = 0.0022), cavity area (P = 0.0001) and cardiomyocyte thickness (P = 0.0001). Diabetic saline group demonstrated a reduction in left ventricular (LV) wall, interventricular (IV) septum, cardiomyocyte thickness and an increase in cavity area, associated with a reduction in LV fractional shortening (P < 0.05), and an increase in LViv relaxation time (P < 0.05). Survival rate decreased from 80% in DS group to 40% in DE group. In conclusion, alloxan diabetes did not affect RV hypertrophy secondary to chronic emphysema, even in the presence of insulin. Diabetes per se induced left ventricular dysfunction, which was less evident in the presence of RV hypertrophy. Survival rate was substantially reduced as a consequence, at least in part, of the coexistence of RV hypertrophy and diabetic cardiomyopathy.

Right ventricular remodeling, its correlates, and its clinical impact in hypertrophic cardiomyopathy.

Structural right ventricular (RV) abnormalities are present in a substantial proportion of patients with hypertrophic cardiomyopathy (HCM), but the trigger for RV hypertrophy remains unclear. The aim of this study was to assess the relationship between RV and left ventricular (LV) remodeling and the impact of biventricular involvement on clinical status in this setting. Ninety-nine patients with HCM and 30 normal subjects with a similar age and gender distribution were prospectively enrolled. Comprehensive echocardiography was performed in all, including the assessment of LV and RV function by tissue Doppler and speckle-tracking echocardiography. Measurement of RV free wall thickness (RVWT) was performed at end-diastole, in a zoomed subcostal view, focusing on the RV midwall. Patients with HCM had increased RVWT (6.4±1.9 vs 3.6±0.8mm, P<.001) and lower values of RV global longitudinal strain (-19.4±4.4% vs -23.8±2.7%, P<.001) compared with control subjects. RVWT was independently related to LV mass and LV global longitudinal strain. Increased RVWT was correlated with New York Heart Association class (r=0.20, P=.04) and calculated sudden cardiac death risk score (r=0.52, P<.001) and was independently related to the presence of ventricular arrhythmias (odds ratio, 2.02; 95% CI, 1.28-3.19; P=.002). In patients with HCM, the presence of RV hypertrophy was associated with increased LV mass and reduced LV longitudinal strain, correlated with increased calculated sudden cardiac death risk score, and independently related to the presence of ventricular arrhythmias. These data suggest more severe disease in patients with biventricular HCM.

Utility of Electrocardiogram in the Assessment and Monitoring of Pulmonary Hypertension (Idiopathic or Secondary to Pulmonary Developmental Abnormalities) in Patients ≤18 Years of Age

Electrocardiograms have utility in disease stratification and monitoring in adult pulmonary arterial hypertension (PAH). We examined the electrocardiographic findings that are common in pediatric PAH and assessed for correlation with disease severity and progression. We retrospectively identified patients aged≤18 years followed at a single institution from January 2001 to June 2012 with catheterization-confirmed diagnosis of idiopathic PAH and PAH secondary to pulmonary developmental abnormalities. Patients with an electrocardiography performed within 60 days of catheterization were included. Primary and secondary outcomes are the prevalence of abnormal electrocardiographic findings at the time of catheterization and the association between electrocardiographic and hemodynamic findings and electrocardiographic changes with disease progression on follow-up catheterization, respectively. Of the 100 electrocardiography-catheterization pairs derived from the 46 patients identified, 93% had an electrocardiographic abnormality: 78% had right ventricular hypertrophy (RVH) and 52% had right axis deviation (RAD) for age. In patients with idiopathic PAH, the presence of RVH and RAD correlated with pulmonary vascular resistance and transpulmonary gradient. RAD and RVH on baseline electrocardiogram was associated with an increased risk of disease progression on subsequent catheterization (odds ratio 11.0, 95% confidence interval 1.3 to 96.2, p=0.03) after adjusting for PAH subgroup. The sensitivity, specificity, and positive and negative predictive values of RAD and RVH on baseline electrocardiogram for disease progression were 92%, 48%, 33%, and 95%, respectively. In conclusion, electrocardiographic abnormalities are common in pediatric PAH. RAD and RVH on electrocardiogram were associated with worse hemodynamics, whereas their absence is suggestive of a lack of disease progression.

Circulation Editors’ Picks

<i>Circulation</i> Editors’ Picks

Right Ventricular Structure Is Associated With the Risk of Heart Failure and Cardiovascular Death

Background— Changes in right ventricular (RV) morphology are associated with morbidity and mortality in heart and lung disease. We examined the association of abnormal RV structure and function with the risk of heart failure or cardiovascular death in a population-based multiethnic sample free of clinical cardiovascular disease at baseline. Methods and Results— The Multi-Ethnic Study of Atherosclerosis (MESA) performed cardiac magnetic resonance imaging on 5098 participants between 2000 and 2002 with follow-up for incident heart failure and cardiovascular death (“death”) until January 2008. RV volumes and mass were available for 4204 participants. The study sample (n=4144) was 61.4±10.1 years old and 47.6% male. The presence of RV hypertrophy (increased RV mass) was associated with more than twice the risk of heart failure or death after adjustment for demographics, body mass index, education, C-reactive protein level, hypertension, and smoking status (hazard ratio, 2.52; 95% confidence interval, 1.55–4.10; P &lt;0.001) and a doubling (or more) of risk with left ventricular mass at the mean value or lower ( P for interaction=0.05). Conclusions— RV hypertrophy was associated with the risk of heart failure or death in a multiethnic population free of clinical cardiovascular disease at baseline.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Left and right ventricular hypertrophy at autopsy of hypertensive individuals

Summary Objective To measure the right and left ventricular thickness in deceased individuals with a history of hypertension submitted to clinical autopsies. Methods We selected 90 cases from the Death Verification Service of the city of Recife, state of Pernambuco, Brazil, of both sexes, with a history of essential arterial hypertension related to heart wall thickness, in addition to correlation with autopsy findings and other clinical reports. Results There was a significant association between the presence of left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH) and between severe hypertensive cardiomyopathy and RVH. There was a predominance of RVH and LVH in men aged 60–79 years and a higher prevalence in the Brazilian mulatto and Black ethnic groups and in those with adequate nutritional status or overweight and obese individuals. Conclusion It was observed that the presence of RVH was related to LVH, suggesting that there are similar pathogenic factors involved in the development of bilateral hypertrophy. The RVH seems to be associated with more severe heart disease and may, based on other studies, be considered as a new prognostic factor in the evaluation of hypertensive patients.

A standard echocardiographic and tissue Doppler study of morphological and functional findings in children with hypertrophic cardiomyopathy compared to those with left ventricular hypertrophy in the setting of Noonan and LEOPARD syndromes

Several clinical and echocardiographic studies describe morphological and functional findings in patients with hypertrophic cardiomyopathy. Less is known regarding morphological and functional characteristics of the left ventricular hypertrophy found in the setting of the Noonan and LEOPARD syndromes. To compare non-invasively the morphological and functional findings potentially affecting symptoms and clinical outcome in children with hypertrophic cardiomyopathy as opposed to Noonan and LEOPARD syndromes. We studied by echo-Doppler 62 children with left ventricular hypertrophy, dividing them into two subgroups matched for age and body surface area. The first group, of 45 patients with a mean age of 7.5 +/- 5.2 years and body surface area of 0.9 +/- 0.44 mq, had idiopathic hypertrophic cardiomyopathy. The second group, of 17 patients, all had left ventricular hypertrophy in the setting of Noonan or LEOPARD syndromes. Their mean age was 6.6 +/- 5 years, and body surface area was 0.8 +/- 0.36 mq. In all patients, we assessed the left ventricular maximal mural thickness, expressed as a Z-score, along with any obstructions in the left and right ventricular outflow tracts. In addition, to define left ventricular diastolic function, we used mitral flow and pulsed Tissue Doppler to record the Ea, Aa, Ea/Aa, E/Ea indexes in the apical 4-chamber view at the lateral corner of the mitral annulus. We also measured the diameters of the coronary arteries in the diastolic frame. Compared to those with hypertrophic cardiomyopathy, those with syndromic left ventricular hypertrophy showed a significantly increased Z-score for mural thickness, and a higher prevalence of obstruction in the left ventricular outflow tract. In addition, the patients with Noonan or LEOPARD syndromes showed a significantly decrease of Ea and increase of Aa, with a decreased Ea/Aa ratio, all suggestive of left ventricular abnormal relaxation. Moreover, the E/Ea ratio was significantly increased in these patients. The presence of right ventricular hypertrophy, mainly associated with dynamic obstruction in the outflow tract, was detected in only 5 of the 17 patients with Noonan or LEOPARD syndromes, as was dilation of the coronary arteries. Compared to children with hypertrophic cardiomyopathy, those with left ventricular hypertrophy in the setting of Noonan or LEOPARD syndromes show more ventricular hypertrophy and diastolic dysfunction, due to both abnormal relaxation and reduced compliance. They also exhibit an increased prevalence of obstruction of the left ventricular outflow tract, along with dynamic obstruction of the right ventricular outflow tract and dilated coronary arteries. These morphological and functional findings could explain the different symptoms and clinical events, and potentially define the more appropriate therapeutic options in children with left ventricular hypertrophy of different aetiology.

Right Ventricular Involvement in Fabry Disease

The aim of the study was to describe right ventricular (RV) structural and functional changes in Fabry disease (FD). A detailed echocardiographic examination was performed in 58 patients with proven FD (mean age 40 +/- 16 years, 24 men). RV hypertrophy (RVH) was present in 40% of affected subjects with similar prevalence in both genders. Approximately two thirds of patients with left ventricular hypertrophy (LVH) also exhibited RVH. RV dilatation was not present in any subject. RV systolic dysfunction was noted in only 1 female subject. RV diastolic dysfunction was present in 47% of 45 subjects in whom RV filling was assessed. RV diastolic dysfunction was associated with the presence of RVH. A significant correlation between RV wall thickness and age (r = 0.52, P < .001) and left ventricular mass index (r = 0.70, P < .001) was noted. RVH with normal chamber size and preserved systolic but impaired diastolic function represents a typical RV structural change in FD. Its prevalence and degree are related to the prevalence and degree of LVH and the age of the patient.

Severe ductal constriction in the third‐trimester fetus following maternal self‐medication with nimesulide

This was a multicenter series of 10 cases of constriction of the fetal ductus arteriosus occurring after maternal ingestion of one or two oral doses of nimesulide, which led to emergency delivery in four cases. The computerized databases of three referral centers were searched for all cases of ductal constriction detected during the last 8 years in association with maternal ingestion of nimesulide. Ten cases were retrieved and represent the study population. The following variables were analyzed: gestational age at diagnosis, reason for nimesulide ingestion, total nimesulide dose, time interval between drug intake and ultrasound examination, indication for echocardiography, presence of right ventricular hypertrophy, presence of tricuspid valve regurgitation, ductal systolic and diastolic peak velocities, ductal pulsatility index, signs of fetal heart failure, pregnancy and feto-neonatal outcome, and ductal status at neonatal echocardiography. Nimesulide ingestion was the result of self-medication in all cases. The mean gestational age at diagnosis was 36.3 weeks and the mean time interval between nimesulide intake and echocardiographic examination was 2.9 days. The five cases with ductal peak velocities > 2.5 m/s showed right ventricular dysfunction with significant tricuspid regurgitation. At echocardiography performed immediately after birth, the ductus appeared closed in all cases and two neonates showed persistent pulmonary hypertension requiring intermittent positive pressure ventilation and nitric oxide therapy for 1 week. Although the true incidence of the adverse effect of nimesulide ingestion during pregnancy cannot be deduced, we believe that patients and their clinicians should be alerted to the possibility that clinically significant ductal constriction may follow maternal self-medication with just one or two oral doses of nimesulide, at least if the drug is taken near term.

Echocardiographic measurement of right ventricular wall thickness in hypertrophic cardiomyopathy: Relation to clinical and prognostic features

Hypertrophic Cardiomyopathy is characterized by unexplained left ventricular hypertrophy. It is uncertain, however, to what extent the right ventricle is also thickened. Right ventricular hypertrophy is found at autopsy in patients who die suddenly but, until recently, systematic evaluation of right ventricular morphology has not been feasible. In this two-dimensional echocardiographic study, a total of 4 to 10 (median 7) right ventricular wall thickness measurements were made from six right ventricular views in 73 patients with hypertrophic cardiomyopathy. Fortyone normal subjects were also studied for comparison.Thirty-two (44%) of the 73 patients had right ventricular hypertrophy with at least two of the wall thickness measurements exceeding 2 standard deviations (SD) from the mean value in the normal subjects. Right ventricular hypertrophy was mild (≤ mm) in 24 patients, moderate (9 to 12 mm) in 7 and severe (>12 mm) in 1. The coefficient of variation of right ventricular wall thickness measurements was similar in normal subjects and patients with and without right ventricular hypertrophy (17 ± 7, 11± 8 and 10 ± 8, respectively). The hypertrophy was concentric, with a current of variation of 25% in all but one patient. There was a strong correlation of maximal right and mean left ventricular wall thickness (r = 0.643, p < 0.001).Right ventricular hypertrophy was not associated with the occurrence of secondary pulmonary hypertension, but was more common in patients with dyspnea on exertion (p < 0.05), severe left ventricular hypertrophy (p < 0.007), supraventricular arrhythmias (p < 0.005) and ventricular tachycardia (p = 0.02) during electrocardiographic monitoring. Stepwise logistic regression analysis revealed that mean left ventricular wall thickness and supraventricular arrhythmias were independent risk factors for right ventricular hypertrophy. Thus, the presence of right ventricular hypertrophy was associated with more severe disease.

Cardiodynamic effects of experimental right bundle branch block in canine hearts with normal and hypertrophied right ventricles

Cardiodynamic effects of acute experimental right bundle branch block (RBBB) were studied in canine hearts: group A included 15 normal hearts; group B-1 had seven hearts with mild right ventricular hypertrophy (RVH), and group B-2 had 11 hearts with marked RVH. The main sequential changes following RBBB were marked prolongation of the Q upstroke interval of the right ventricle and striking shortening of right ventricular systolic time that affected right and left ventricular interaction, particularly in the hearts with RVH. Hemodynamic changes were: the right ventricular end-diastolic pressure was elevated markedly (4.4 ± 2.2 → 9.8 ± 2.6 mm Hg, p < 0.001) in group B-2, moderately ( p < 0.01) in group B-1, and not at all in group A. The right ventricular positive peak dp dt decreased remarkably (1036 ± 151 → 827 ± 152 mm Hg/sec, p < 0.001) in group B-2 and negligibly in the other groups. A significant correlation existed between the percentage of decrease in right ventricular peak dp dt and the QRS duration of RBBB in each group ( p < 0.01). The left ventricular peak negative dp dt decreased distinctly (2570 ± 326 → ± 2055 ± 362 mm Hg/sec, p < 0.01) in group B-2 and not at all in the other groups. The atroke volume showed 12% decrease in group B-2 ( p < 0.001), 8% decrease in group B-1 (NS), and no decrease in group A. In the presence of RVH, acute RBBB causes significant impairment of right and left ventricular function. The magnitude of the impairment invariably depends upon both the prior degree of RVH and the width of the QRS complex.

Echocardiographic detection of right ventricular hypertrophy

M-mode echocardiographic right ventricular wall thickness (RVW) and diastolic right ventricular internal diameter (RVID), when above the accepted normal range (RVW ≤ 5 mm, RVID ≤ 26 mm), are frequently used clinically to predict the presence of right ventricular hypertrophy. RVID was compared to anatomic right ventricular mass (RVM) in 27 patients and to RVW in 13 patients to determine their accuracy for predicting right ventricular hypertrophy (RVM > 65 gm). When increased, both measurements were specific for right ventricular hypertrophy. The specificity for RVW above 5 mm was 100% and for RVID greater than 26 mm was 79%. Neither was a sensitive indicator of hypertrophy. Only 36% of those with anatomic right ventricular hypertrophy had an echocardiographically dilated ventricle, and 67% had a thickened free wall. Neither measurement proved to be an accurate predictor of RVM, with a correlation for RVW of 0.56 and for diastolic RVID of 0.19.

Effects of duration and severity of arterial hypertension and cardiac hypertrophy on coronary vasodilator reserve.

Cardiac hypertrophy is associated with a decrease in coronary reserve. However, factors which may modulate the interaction between myocardial growth and vascular proliferation, such as duration and severity of hypertrophy, have not been evaluated. We measured myocardial perfusion with microspheres in conscious, chronically instrumented. Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats at 3, 7, and 15 months of age; and in SHR stroke-prone (SHR-SP) rats at 13-14 months of age. Myocardial perfusion was measured with microspheres in awake rats at rest and during maximal coronary dilation produced by dipyridamole infusion (2.0 mg/kg per min, iv). Arterial pressure was significantly elevated (P less than or equal to 0.05) in all hypertensive groups (vs. age-matched WKY), both at rest and during dipyridamole infusion. Left ventricular mass in the SHR rats was increased significantly (P less than or equal to 0.05) by 14%, 28%, and 29% at 3, 7, and 15 months, respectively. Left ventricular mass in the SHR-SP group was increased by 50% (P less than or equal to 0.05) compared to the 15-month-old WKY. Left ventricular minimal coronary vascular resistance (per gram) was significantly greater (P less than or equal to 0.05) in SHR at 7 months, and in the SHR-SP group (66% and 60%, respectively). Right ventricular minimal coronary vascular resistance was significantly greater (P less than or equal to 0.05) in SHR at 7 and 15 months (50%), and in the SHR-SP group (122%), compared to 15-month-old WKY. The results indicate the following: (1) the increase in minimal coronary vascular resistance between SHR and WKY rats was greatest when left ventricular hypertrophy peaked (7 months) and was no longer present after left ventricular hypertrophy had stabilized. (2) In 14-month-old SHR-SP rats, with more severe left ventricular hypertrophy and hypertension, minimal coronary vascular resistance was considerably higher than in SHR of approximately the same age. (3) Long-term arterial hypertension was associated with a higher right ventricular minimal coronary vascular resistance. Resistance appeared to change in proportion to the severity of hypertension, and the changes were independent of the presence of right ventricular hypertrophy.

Diagnostic value of visualization of the right ventricle using thallium-201 myocardial imaging.

The diagnostic significance of visualizing the right ventricle on thallium-201 myocardial perfusion scans (T-scan) at rest was studied in 53 patients. In 33 patients the right ventricle was visualized clearly on the T-scan (group A). Hemodynamic evidence of right ventricular hypertension with systolic pressure greater than or equal to 30 mmHg was present in 28 of 33 (85%) of these patients. Right ventricular volume overload with left-to-right shunt greater than 2:1 was present in three patients. Other tests were diagnostic for right ventricular enlargement and or pulmonary hypertension as follows: chest x-ray (58%), echocardiogram (36%) and electrocardiogram (15%). In an unselected group of 20 patients (group B) where resting T-scan did not show visualization of the right ventricle, the right ventricular systolic pressure was less than 30 mm Hg in all. The other noninvasive tests did not reveal presence of right ventricular hypertrophy or enlargement. T-scan appears to be a useful and sensitive test in detecting right ventricular pressure or volume overload compared with other noninvasive tests. This may be useful in detection of patients with right ventricular hypertrophy or enlargement secondary to pulmonary hypertension or other causes.