Gary W. Burggraf

Left Ventricular Volume Changes After Amyl Nitrite and Nitroglycerin in Man as Measured by Ultrasound

The therapeutic effect of nitrites in myocardial ischemia is considered to be due in part to a reduction of left ventricular volume but measurement of this parameter in man has been difficult. The technique of echocardiography was used to measure changes in left ventricular end-diastolic volume (LVEDV) and end-systolic volume (LVESV) after administration of amyl nitrite (AN) and nitroglycerin (NG) in 20 normal subjects. Control LVEDV was 131 ± 8 ml (mean ±SEM) and LVESV 30 ± 2 ml. After AN, LVEDV fell 18 ± 2% (P < 0.001) and LVESV by 57 ± 3% (P < 0.001) in 15 sec to 1 min. Heart rate (HR) rose from 68 ± 3 to 108 ± 4 beats/min at 1 min and blood pressure (BP) fell from 119/69 ± 3/2 to 99/47 ± 4/3 mm Hg. Following NG, LVEDV fell 11 ± 2% (P < 0.001) and LVESV 21 ± 3% (P < 0.001) within 2-5 min. HR rose from 65 ± 2 to 72 ± 3 beats/min and BP fell from 111/67 ± 3/2 to 102/70 ± 5/2 mm Hg at 3 min. Cardiac output increased from 6.9 ± 0.3 to 11 ± 0.9 L/min 30 sec after AN while no significant change occurred with NG. Stroke volume decreased from 101 ± 6 to 93 ± 5 ml/beat 5 min after NG while no significant change occurred after AN. This study has shown that both AN and NG produce significant decreases in LVEDV and LVESV which may contribute to their beneficial effects in myocardial ischemia.

The 'athletic heart syndrome'. A critical review.

SummaryCardiological findings in athletes are often similar to those observed in clinical cases. Electrocardiographic and cardiac imaging abnormalities as well as physical findings may be the same in both of these groups. Bradycardia and rhythm disturbances are the most common abnormalities in athletes. Most athletes with abnormal electrocardiograms are asymptomatic and numerous investigators have failed to detect heart disease in association with such electrocardiograms. In contrast to cardiac dysfunction observed in clinical cases, enhanced or normal ventricular systolic and diastolic function have been reported in athletes. In endurance athletes, this is associated with very high values for maximal aerobic power (V̇O2max).Absolute and body size-normalised cardiac dimensions in most athletes do not approach values from chronic disease states, and may not exceed echocardiographic normal limits. In addition, pathological and physiological enlargement appear to be biochemically and functionally different. Myosin ATPase enzyme expression and calcium metabolism are different in rats with pathologically or physiologically induced enlargement. The reported biochemical differences underlie systolic and diastolic dysfunction in pathological enlargement. Conversely, trained rodents and humans have demonstrated enhanced systolic and diastolic function. It is important to note that cardiac enlargement observed in athletes is the result of normal adaptation to physical conditioning and/or hereditary influences. Conversely, pathological changes result from disease processes which can lead in turn to reduced function, morbidity and mortality.Since the mid 1970s echocardiography has been used to compare cardiac dimensions in male endurance- and resistance-trained athletes. A sport-specific profile of eccentric and concentric enlargement has been documented in endurance and resistance athletes, respectively. Subsequent studies of athletes have examined factors such as age, sex and degree of competitive success to determine their contribution to these sport-specific cardiac profiles. Unique athletic subgroups have also been analysed and have included ballet dancers, rowers, basketball players and triathletes. However, there is a paucity of data on cardiac dimensions in female athletes. Finally, physical conditioning studies have also examined echocardiographic dimensions before and after endurance and resistance training. Significant enlargement of internal dimensions, wall thickness or left ventricular mass have been reported but such increases are relatively small and by no means universal.Several conflicting explanations for enlarged cardiac dimensions appear in the literature. Chronic volume and pressure haemodynamic overloading during physical conditioning has been proposed to explain eccentric and concentric cardiac enlargement in endurance- and resistance-trained athletes respectively. However, twin studies suggest that hereditary factors may be important determinants of cardiac dimensions and/or the degree of cardiac adaptability to physical conditioning.Another body of research has suggested the possibility that endocrine effects related to normal growth and/or physical conditioning may stimulate cardiac enlargement. Thyroid hormone, catecholamines, growth hormone and testosterone can alter cardiac dimensions and their blood levels are elevated with exercise. However, their influence on myocardial structure in athletes has not yet been clarified. In this regard, blood testosterone levels increase transiently following acute exercise bouts in young men and may contribute to the process of skeletal muscle hypertrophy. Significant statistical associations have been reported between skeletal and cardiac muscularity. Therefore, a common influence of testosterone or other hormones on skeletal and cardiac muscle hypertrophy has been hypothesised and may account for hereditary and/or conditioning induced cardiac enlargement in athletes. Future investigations should reassess the role of haemodynamic stress and clarify the quantitative role of heredity and endocrine factors in determining cardiac dimensions. In this way a clearer indication may be deduced as to the mechanism(s) involved in the apparent moderate cardiac enlargement reported in athletes. Research should first describe the cardiac profile of a wide range of female athletes and then determine the cause of any potential gender-based differences in cardiac size and adaptation to exercise.

Electrocardiographic and echocardiographic characteristics of female athletes.

This study examined electrocardiographic and echocardiographic characteristics of endurance- and resistance-trained female athletes. The subjects were 10 varsity caliber endurance-trained athletes, 10 resistance-trained athletes, and 10 nonathletes. Data collection included anthropometric measurements, VO2max, standard 12-lead ECGs and left ventricular dimensions measured by M-mode and two-dimensional echocardiography. For endurance-trained athletes, absolute left ventricular end-diastolic volume and values normalized for lean body mass were significantly greater than in nonathletes. An interstudy comparison of female vs male endurance-trained athletes from the same population also revealed significantly lower values for M-mode left ventricular mass expressed per kilogram of lean body mass in the former. Absolute and normalized wall thicknesses were not significantly greater in resistance-trained athletes compared to the other two groups. Wall thickness indexed for lean body mass was similar for the three groups. Sinus bradycardia was observed in all endurance athletes and in four resistance-trained athletes. ECG criteria were unreliable for the prediction of left ventricular enlargement. It appears that both female resistance- and endurance-trained athletes exhibit a lesser degree of enlargement of left ventricular wall thickness and mass than male athletes. A close relationship between skeletal and cardiac muscularity in resistance-trained athletes of both genders also was supported.

Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of left bundle branch block: an echocardiographic study.

This study tests the electrocardiographic diagnosis of left ventricular (LV) hypertrophy in the presence of left bundle branch block (BBB). The LV mass of 125 patients with left BBB was estimated by echocardiography. M-mode echocardiography was technically adequate in 80% of patients. LV mass was calculated using previously validated M-mode formulas and then indexed to body surface area. The known shifts in the QRS voltage and axis with the onset of left BBB led to the selection of 4 electrocardiographic parameters for the diagnosis of LV hypertrophy: R in aVL 11 or more; QRS axis -40 degrees or less (or SII greater than RII); SV1 + RV5 to RV6 40 or more; SV2 30 or more and SV3 25 or more; these parameters were used in cumulative fashion. This cumulative approach was superior to using single conventional criterion such as the SV1 + RV5 or RV6. When LV hypertrophy was defined as an M-mode index of at least 115 g/m2, the sensitivity was 75% and specificity 90%. Using an M-mode mass of at least 215 g as the standard, the sensitivity was 73% and the specificity 66%. LV hypertrophy can be diagnosed by electrocardiographic criteria in the presence of left BBB at least as reliably as in normal conduction.

Echocardiographic assessment of tricuspid regurgitation during ventricular demand pacing

Twenty patients from our pacemaker clinic population were assessed clinically and by saline contrast echocardiography (subxiphoid view) to determine the prevalence of tricuspid regurgitation (TR) and, if TR was present, its mechanism. The patients had no known TR before lead placement, a single transvenous right ventricular pacing lead present more than 6 months (mean 52, range 7 to 138), ventricular demand pacing alternating with sinus rhythm and rate programmability. Each patient was studied in sinus rhythm and during ventricular pacing. Using the criterion of inferior vena cava (IVC) contrast reflux during ventricular systole to diagnose TR, no patient had evidence of TR in sinus rhythm, consistent with clinical examination. During ventricular demand pacing, jugular venous pulse cannon A waves developed in 10 patients, and 18 patients (including these 10) had IVC contrast reflux during ventricular systole. Analysis of the timing of IVC reflux revealed its close temporal relation to the timing of atrial systole rather than a fixed timing during ventricular systole. This reflux occurred with loss of normal atrioventricular (AV) synchrony and the underlying mechanism in all cases was shown to be right atrial contraction against a closed tricuspid valve. Two patients who did not have such a pattern with pacing maintained normal AV synchrony. These observations indicate that: TR is an uncommon accompaniment of ventricular demand pacing; the jugular venous pulse and IVC echocardiographic contrast patterns during ventricular demand pacing simulate TR when AV asynchrony [corrected] occurs; and the IVC contrast pattern of pacing induced AV asynchrony [corrected] is best termed the cannon A wave synchronous pattern.

Structure and process measures of quality of care in adult congenital heart disease patients: A pan-Canadian study

BACKGROUND There are more adults than children with congenital heart disease. Of over 96,000 ACHD patients in Canada, approximately 50% require ongoing expert care. In spite of published recommendations, data on the quality of care for ACHD patients are lacking. METHODS Survey methodology targeted all Canadian Adult Congenital Heart (CACH) network affiliated ACHD centers. Clinics were asked to prospectively collect outpatient and procedural volumes for 2007. In 2008, centers were surveyed regarding infrastructure, staffing, patient volumes and waiting times. RESULTS All 15 CACH network registered centers responded. The total number of patients followed in ACHD clinics was 21,879 (median per clinic=1132 (IQR: 585, 1816)). Of the total 80 adult and pediatric cardiologists affiliated to an ACHD clinic, only 27% had received formal ACHD training. Waiting times for non-urgent consultations were 4 ± 2 months, and 4 ± 3 months for percutaneous and surgical procedures. These were beyond Canadian recommended targets at 11 sites (73%) for non-urgent consultations, at 8 sites (53%) for percutaneous interventions and 13 sites (87%) for surgery. CONCLUSIONS Of a minimum number of 96,000 ACHD patients in Canada, only 21,879 were being regularly followed in 2007. At most sites waiting times for ACHD services were beyond Canadian recommended targets. In spite of universal health care access, published guidelines for ACHD patient structure and process measures of health care quality are not being met.

Prediction of left ventricular mass from the electrocardiogram

Multiple stepwise regression methods were used to derive electrocardiographic (ECG) models for prediction of the echocardiographic left ventricular (LV) mass index from standard 12-lead ECG measurements using data files of 203 men and 252 women. The correlation between echocardiographic and ECG estimates of LV mass index was R2 = 0.58 for men and R2 = 0.42 for women. A separate logistic regression model was derived for classification of LV hypertrophy as a dichotomized dependent variable. This classifier chose R (aVL), T (V6), and S (V1) for men and R (aVL), T (V6), and S (I) for women and produced a moderate sensitivity (53.7% for men and 63.4% for women) and specificity (94.9% for men and 92.9% for women). We conclude that the initial performance of these and other recently developed multivariate estimators of LV mass and LV hypertrophy classifiers is promising enough to subject them to further studies to evaluate their utility as risk predictors.

Mitral valve motion and changes in left ventricular end-diastolic pressure: A correlative study of the PR-AC interval

To evaluate the relation between mitral valve motion and left ventricular end-diastolic pressure, the PR-AC interval, an index derived from the electrocardiogram and mitral echogram, and the left ventricular endodiastolic pressure were determined simultaneously in 22 patients undergoing diagnostic cardiac catheterization. Intravenous infusion of dextran or administration of nitroglycerin was used to alter left ventricular end-diastolic pressure to determine if there was a predictive relation between this pressure and the PR-AC interval during acute hemodynamic manipulations. There was a weak negative correlation (r = -0.33, P less than 0.01) between this pressure and the PR-AC interval. At rest a PR-AC interval greater than 0.06 second correctly predicted a left ventricular end-diastolic pressure of less than 20 mm Hg in 15 of 16 subjects. However, in four of six subjects with a PR-AC interval of 0.06 second or less, the end-diastolic pressure was less than 20 mm Hg. After interventions that varied left ventricular end-diastolic pressure by a factor of 2, the PR-AC interval changed slightly or not at all. These data suggest that the PR-AC interval is of limited value in predicting abnormal values or serial changes in left ventricular end-diastolic pressure.

The impact of the computer-reported vectorcardiogram on the cardiologist interpreter of the scaler electrocardiogram*

The purpose of this study was to determine if the computer-reported vectorcardiogram (VCG) had a notable impact on the cardiologist interpreter of the 12-lead scalar electrocardiogram (ECG). Three cardiologists read 100 12-lead scalar ECGs and four months later again read the same tracings while having available the VCG computer report. The diagnosis was altered in 25% of the repeated interpretations. Forty-five per cent of these had only minor changes and can probably be disregarded. Major or significant changes occurred in 14% of the records, and 80% of these were apparently attributable to the computer report. It was concluded that the use of a computer-assisted interpretation of a VCG may enhance the uniformity and consistency of the cardiologists interpretation of the scalar ECG.