Left ventricular function at rest and during Raynaud's phenomenon in patients with scleroderma

We evaluated left ventricular function in 10 scleroderma patients with signs and symptoms suggestive of congestive heart failure. M-mode and two-dimensional echocardiography demonstrated normal to increased systolic function in all patients. The presence of pulmonary venous congestion on the chest radiograph was not useful in assessing left ventricular systolic function. Five of nine patients with normal to increased left ventricular ejection fraction (LVEF) had increased cardiothoracic ratios and increased pulmonary vascular markings. Left ventricular hypertrophy was associated with a worse New York Heart Association functional class, more pulmonary vascular congestion, and greater left atrial size. In the presence of normal systolic function and ventricular hypertrophy, diminished left ventricular diastolic compliance may account for the cardiac dysfunction in these patients. Cold pressor testing induced peripheral Raynaud's phenomenon in nine of nine patients; however, no ST segment changes or chest pain was provoked. In seven of nine patients there was no abnormal fall in LVEF. The mechanism for the fall in ejection fraction seen in two patients may be related to an increase in afterload or myocardial ischemia secondary to coronary atherosclerosis. We found little to suggest that a myocardial Raynaud's phenomenon affects left ventricular perfusion or systolic function. Clinical signs and symptoms of congestive failure as well as chest radiographs are poor indicators of impaired systolic function in scleroderma patients. Based on these findings, it appears that evaluation of left ventricular systolic function should include echocardiographic or angiographic study before such patients are treated for heart failure with inotropic agents.     

Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy

Left ventricular hypertrophy due to aortic stenosis, hypertension and other forms of heart disease is associated with abnormalities of diastolic function. It is uncertain whether these changes are an inherent consequence of the hypertrophic process or represent additional pathologic factors. To investigate this issue, echocardiographic indexes of left ventricular early diastolic function in highly trained athletes were compared with those in age-matched normal control subjects. Athletes were equally classified into two groups: 11 swimmers who had a pattern of myocardial hypertrophy with normal wall thickness to dimension ratio and 11 power lifters whose wall thickness to dimension ratio was increased. The peak rates of left ventricular dimension increase and wall thinning in swimmers and power lifters were greater than in control subjects despite significantly higher left ventricular wall thickness and left ventricular mass index in the athletes. This increase in diastolic function indexes was associated with greater ventricular size and systolic performance. Normalization of the peak rate of dimension increase for end-diastolic dimension and adjustment of the peak rate of wall thinning for the fractional systolic thickening resolved any differences between groups. Thus, after the effects of ventricular size and systolic function were taken into consideration, diastolic function was normal in these subjects with considerable physiologic hypertrophy. This is in contrast to the findings in patients with hypertrophy associated with left ventricular pressure or volume overload, and suggests that abnormalities of diastolic function seen in pathologic hypertrophy are due to factors other than cardiac hypertrophy itself.     

Effect of left ventricular hypertrophy secondary to systemic hypertension on left coronary artery flow dynamics.

STUDY OBJECTIVE--The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. DESIGN--Measurements of blood velocities in the left anterior descending coronary artery were made with a 20 MHz Doppler catheter with a top mounted annular crystal. All patients had normal coronary arteriograms. PATIENTS--23 hypertensive patients [systolic/diastolic pressure: 181(SD 15)/100(4) mm Hg)] with left ventricular hypertrophy, and 13 atypical chest pain patients without left ventricular hypertrophy or any abnormal haemodynamic findings (normal controls) entered the study. MEASUREMENTS AND MAIN RESULTS--The left anterior descending coronary artery blood velocity waveform in pressure overloaded left ventricular hypertrophy was characterised by delayed early diastolic inflow. The diastolic rise time of coronary flow (TDR), ie, the time from the beginning of diastole to peak velocity, was higher in patients with hypertensive left ventricular hypertrophy than in normal controls, at 145(56) v 66(15) ms, p less than 0.001. In patients with hypertensive left ventricular hypertrophy, TDR correlated well with the degree of hypertrophy (r = 0.83, p less than 0.01) and also with peak left ventricular systolic pressure (r = 0.62, p less than 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity, decreased with prolongation of TDR (r = 0.58, p less than 0.02). CONCLUSIONS--(1) Impairment of early diastolic coronary arterial inflow is the most remarkable characteristic in pressure overloaded left ventricular hypertrophy; (2) preceding systolic vascular compression and impaired left ventricular relaxation correlate with the delayed early diastolic inflow; (3) the delayed inflow is an important possible cause of the decreased coronary flow reserve in the hypertensive left ventricular hypertrophy.     

Echocardiographic features of supracristal ventricular septal defect with prolapsed aortic valve leaflet.

Anatomically diagnostic echocardiographic features of a supracristal ventricular septal defect with prolapsed right coronary aortic leaflet are described in four children aged 2 to 10 years. Both single crystal M mode as well as 80 ° phased array sector scan techniques were used. The echographic features in the M mode scan from the aorta to the left ventricle in three of four patients included (1) the position of the ventricular septal defect as a clear space between the interrupted septal echoes below the aortic root, and (2) the prolapsed right coronary aortic leaflet as anomalous linear echoes in the right ventricular outflow tract. Angiographic, intraoperative and echocardiographic contrast studies were used to establish the diagnosis.On sector scanning using the long axis view, the supracristal ventricular septal defect was recognized as a clear space between the top of the ventricular septum and the anterior segment of the aortic root in three of four patients. The right coronary aortic leaflet was seen to prolapse into the right ventricular outflow tract through this defect, and its motion could be clearly followed during systole and diastole. It is concluded that echocardiography provides anatomic diagnosis of this lesion. Furthermore, the severity and progression of this lesion can be assessed by quantitation of the left ventricular size and performance.     

Right ventricular diastolic pressure in coronary artery disease

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P < 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P < 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P < 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.     

Myocardial contractile function of the left ventricle in patients with congenital stenosis of the ostium aortae

A study of 61 patients with congenital stenosis of the aortic ostium has shown that left ventricular myocardial dysfunction is related to the extent of myocardial hypertrophy. Progressive discrepancy between growing left ventricular myocardial hypertrophy and its blood supply resulted, at a certain point, in a qualitative change from compensatory to abnormal hypertrophy. The extent of left ventricular hypertrophy determined the severity of aortic stenosis and left ventricular dysfunction. The emergence of electrocardiographic signs of left ventricular hypertrophy and systolic overstrain is indicative of the defect acquiring a new quality--that of left ventricular and relative coronary insufficiency.     

Hypertrophic cardiomyopathy after aortic valve replacement

The association of hypertrophic cardiomyopathy and aortic valve disease is well documented. However, the new development of the syndrome late after valve replacement has not previously been described. We present six cases, all occurring in women aged 50 to 71 years who had evidence of hypertrophic cardiomyopathy 3 to 5 years after successful valve replacement. The preoperative hemodynamic lesion was aortic stenosis in four and aortic regurgitation in two. Before operation no patient showed evidence of hypertrophic cardiomyopathy as judged by the absence of (1) asymmetric septal hypertrophy (the septal/posterior wall ratio was less than 1.4:1.0 in each case); (2) systolic anterior mitral valve motion; (3) obliteration of the left ventricular cavity on angiography; and (4) an intraventricular pressure gradient. After valve replacement no patient had significant aortic regurgitation or was hypertensive. Four patients subsequently had recurrence of symptoms including dyspnea in four, angina in three and syncope in two. The electrocardiogram revealed reappearance of left ventricular hypertrophy in four patients and left bundle branch block in one. The echocardiogram disclosed asymmetric septal hypertrophy in six (septal/posterior wall ratio greater than 1.8:1.0), systolic anterior motion in three and evidence of inflow obstruction in three. At cardiac catheterization an intraventricular gradient of 36 to 60 mm Hg was demonstrated at rest in three patients, on provocation in one patient; two patients showed no gradient. Angiograms showed obliteration of the left ventricular cavity in all six patients (ejection fraction 0.84 to 0.93). Two patients had coronary artery disease. No patient had an aortic transvalve gradient at rest or with exercise.     

Hemodynamics in endomyocardial fibrosis

Nine patients with endomyocardial fibrosis have been studied. The clinical diagnosis was confirmed by right ventricular angiography in all of them. They were submitted to right and left ventricular catheterization and had the cardiac pressures, the pulmonary arteriolar resistance, and the cardiac index measured. The ratio between the end-diastolic and systolic ventricular pressures has been taken as an index of the degree of impairment to ventricular filling, and, based on this, patients were classified into two groups: I, predominant or isolated right ventricular disease (seven patients); and II, predominant left ventricular disease (two patients).Group I patients were characterized by a right ventricular $\text{D}{}_2\text{S}$ ratio above 60 per cent, severe tricuspid regurgitation, a diastolic pulmonary artery pressure slightly lower than the right ventricular plateau and end-diastolic pressures, and a reversal of the gradient between the left ventricular end-diastolic pressure and the right atrial mean pressure; these two latter findings strongly suggesting a diastolic blood flow between the right atrium and the left ventricle.The two patients in Group II did not show evidences suggestive of tricuspid regurgitation or of an early opening of the pulmonic valve. Even presenting high values for the left ventricular $\text{D}{}_2\text{S}$ ratio, the pulmonary arteriolar resistance was normal in one patient and mildly elevated in the other patient.     

Factors affecting left ventricular remodelling and mechanics in the long-term follow-up after successful repair of aortic coarctation

AIMS: To identify factors predisposing to abnormal left ventricular geometry and mechanics in 52 patients after successful repair of aortic coarctation. METHODS AND RESULTS: We evaluated left ventricular remodelling, systolic midwall mechanics, and isthmic gradient by echo-Doppler, systemic blood pressure at rest/exercise and by ambulatory blood pressure monitoring, and the aortic arch by magnetic resonance imaging. Echocardiographic findings were compared with those of 142 controls. The patients with aortic coarctation showed an increased indexed left ventricular end-diastolic volume, increased mass index, increased ratio of mass to volume and systolic chamber function. The contractility, estimated at midwall level, was increased in 21 percent of the patients. In 26 (50 percent) of the patients, we found abnormal left ventricular geometry, with 9 percent showing concentric remodelling, 33 percent eccentric hypertrophy, and 8 percent concentric hypertrophy. These patients were found to be older, underwent a later surgical repair, and to have higher systolic blood pressures at rest and exercise as well as during ambulatory monitoring. The relative mural thickness and mass index of the left ventricle showed a significant correlation with different variables on uni- and multivariate analysis. Age and diastolic blood pressure at rest are the only factors associated with abnormal left ventricular remodelling. CONCLUSIONS: Patients who have undergone a seemingly successful surgical repair of aortic coarctation may have persistently abnormal geometry with a hyperdynamic state of the left ventricle. This is more frequent in older patients, and in those with higher diastolic blood pressures.     

Profiles of coronary blood flow velocity in patients with aortic stenosis and the effect of valve replacement: a transthoracic echocardiographic study.

OBJECTIVE--To report the first non-invasive assessment by transthoracic Doppler echocardiography of coronary blood flow in patients with aortic stenosis and of the effects of valve replacement. DESIGN--High frequency transthoracic Doppler echocardiography was used to examine resting phasic flow in the left anterior descending coronary artery before and after replacement of the aortic valve in awake, unsedated patients with pure aortic stenosis and normal coronary arteries. SETTING--A tertiary referral cardiothoracic centre. METHODS--Eleven patients with pure aortic stenosis and normal coronary arteries (six men, five women, mean (range) age 69 (50-82) years), were studied the day before and 1 week after replacement of the aortic valve. These patients were selected from a cohort of 15 due to ease of imaging of the left anterior descending coronary artery. Seven had a history of angina. Haemodynamics, peak transvalvar aortic gradient, left ventricular mass index, ventricular dimensions, and profiles of coronary flow velocity were measured. Profiles of coronary flow velocity were also measured in a control population of 10 normal subjects (five men, five women, mean (range) age 58 (34-66) years). RESULTS--The control population showed forward flow throughout systole, but reversed early systolic flow (mean velocity 20.6 (3.6) cm/s) was seen in six patients with aortic stenosis. Only three of these patients had a clinical history of angina. Peak and mean systolic and diastolic forward flow velocities were not significantly different in the control group and in patients with aortic stenosis. The time from the start of systole to the onset of forward systolic flow was significantly longer in patients with aortic stenosis than in the control population (185 (8.5) v 85 (10) ms, p < 0.01). The time from the onset of diastolic flow to peak diastolic velocity was also significantly longer in the aortic stenosis group (146 (16) v 74 (13) ms, p < 0.01). These abnormalities in profiles of coronary flow were reversed by replacement of the aortic valve. There was no correlation between changes in flow profiles in patients with aortic stenosis and preoperative clinical history, transvalvar gradient, left ventricular mass index, or ventricular dimensions. CONCLUSIONS--Coronary flow profiles in patients with aortic stenosis were characterised by reversed early systolic flow and delayed forward systolic flow and attainment of peak diastolic velocity. Reversal of these abnormalities by replacement of the aortic valve may reflect altered left ventricular and aortic haemodynamics and contribute to the relief of angina when left ventricular hypertrophy persists. Further studies may correlate abnormalities of coronary flow with preoperative clinical and haemodynamic state.     

Early diastolic left ventricular function in children and adults with aortic stenosis

Pressure overload hypertrophy of the left ventricle is associated with abnormal left ventricular early diastolic filling. The roles of the extent of cardiac hypertrophy, depressed left ventricular systolic function and aging in the pathogenesis of left ventricular diastolic dysfunction have not, however, been fully defined. To determine the relative importance of these factors in the pathogenesis of diastolic dysfunction in pressure overload hypertrophy, 16 children and 25 adults with aortic stenosis were compared with 48 normal children and adults, using rates of left ventricular early diastolic filling and wall thinning derived from M-mode echocardiography. Left ventricular early diastolic filling and wall thinning rates were significantly depressed in both children and adults with aortic stenosis as compared with values in normal subjects. Filling and thinning rates correlated negatively with age, left ventricular peak systolic pressure and wall thickness in all subjects. Furthermore, the effect of age on diastolic function appeared to be mediated by age-related increases in systolic pressure and wall thickness. In adults with aortic stenosis, early diastolic filling and wall thinning rates were depressed to a similar extent in subjects with normal and abnormal systolic function; thus, diastolic dysfunction does not appear to be a manifestation of abnormal systolic loading and ejection performance. These results suggest that extent of hypertrophy itself plays a dominant role in the mechanism of impaired left ventricular early diastolic filling in pressure overload due to aortic stenosis.     

Long-term hemodynamic function of the transplanted heart

The aim of this study was to identify the long-term haemodynamic changes of the transplanted heart. Between 1987 and 1997, 136 patients required cardiac transplantation at Dijon hospital. During follow-up, 76 patients aged 51.2 +/- 9.46 years underwent catheter studies (12 women, 15.8%; and 64 men, 84.2%). Right and left heart catheterisation was performed at 3 months, 1, 2, 3 and 5 years after transplantation. Right heart catheterisation included measurement of mean pulmonary artery and pulmonary capillary pressures and pulmonary arteriolar resistances. During left heart catheterisation, cardiac output, mean aortic pressure, the ejection fraction, the dp/dt max of the left ventricular wall, systemic arterial resistances and left ventricular end diastolic pressures were measured. At each catheter study, the indexed myocardial mass, indexed end systolic and end diastolic left ventricular volumes, the mass/volume ratio, the residual serum cyclosporine concentrations and the serum creatinine were analysed. In addition, an endomyocardial biopsy was also performed. Initially raised, the mean pulmonary artery and pulmonary capillary pressures decrease from the 3rd month to the 2nd year. From the 3rd year onwards, they readjust to the upper limits of normal. The pulmonary artery resistances underwent the same changes. The left heart parameters remained constant over the period of follow-up but with a heart rate, mean aortic pressure and left ventricular end diastolic pressure higher than normal. The indexed myocardial mass was increased at all periods. The indexed left ventricular end systolic and diastolic volumes decreased with a M/V ratio which increased. Cyclosporine concentrations decreased whereas serum creatinine increased. The frequency of severe rejection and of coronary atherosclerosis was low. Significant correlations were observed between different parameters at different periods. In the long-term, the function of the transplanted heart is not normal in the strict sense of the term. The apparent normality is obtained by anti-hypertensive treatment. The transplanted heart adapts to the increase in cyclosporine-induced afterload by permanent myocardial hypertrophy, and increased diastolic pressure probably relates to diastolic dysfunction without noticeable intracardiac fibrosis.     

Volume loading improves low cardiac output in experimental right ventricular infarction

To evaluate the effect of volume loading in the low output state associated with right ventricular infarction, isolated right ventricular infarction was produced in seven dogs with the pericardium intact. Volume loading and pericardiotomy were then sequentially performed. After the production of right ventricular infarction, right ventricular systolic pressure decreased by 25%, aortic pressure by 36% and cardiac output by 32%. Right ventricular ejection fraction decreased by 57%, but left ventricular ejection fraction did not change significantly. Left ventricular transmural pressure and diastolic size decreased, and right ventricular diastolic size increased. Intrapericardial pressure increased and equalization of diastolic pressures was noted. Volume loading resulted in increased right ventricular systolic pressure and stroke work, increased aortic pressure and cardiac output and increased transmural pressure and diastolic size in both ventricles. Pericardiotomy resulted in further increases in right and left ventricular filling, stroke work and cardiac output, as well as resolution of equalized diastolic pressures. These results indicate that cardiac output in experimental right ventricular infarction increases with volume loading, which enhances left ventricular preload by augmenting right ventricular output. Elevated intrapericardial pressure affects filling of both ventricles and may play a role in the pathophysiology of low cardiac output in right ventricular infarction.     

Coronary flow studies in patients with left ventricular hypertrophy of the hypertensive type. Evidence for an impaired coronary vascular reserve

Increased myocardial blood flow occurs in ventricular hypertrophy, but flow per 100 grams of myocardium remains normal. The increase in flow may be obtained at the expense of the existing coronary vascular reserve or by an increase in the vascular bed. The coronary vascular reserve was studied by analyzing the hyperemic reaction to selective injection of contrast agent into the coronary arteries in 25 patients: a control group (9 patients) with chest pain syndrome, normal coronary arteries and a normal left ventricle (Group I) and 16 patients with aortic stenosis, left ventricular hypertrophy and normal coronary arteries (Group II). The hyperemic response in Groups I and II was 73.3 +/- 2.2 and 65.8 +/- 9.1 percent, respectively (difference not significant). Group II was subdivided into two groups: Group IIA had five patients with a left ventricular mass of less than 200 g (mean 158.8 +/- 25.9); this group had a hyperemic response of 102.3 +/- 9.9 percent. Group IIB had 11 patients with a left ventricular mass of more than 200 g (mean 308.9 +/- 22.5) and a hyperemic response of 49.27 +/- 10.42 percent. The hyperemic response was correlated with the diastolic left ventricular-aortic gradient (r = +0.64, p less than 0.001), left ventricular mass (r = -0.51, p less than 0.01) and aortic diastolic pressure (r = +0.636, p less than 0.001). Group I had a left ventricular mass similar to that of Group IIA (124.9 +/- 9 and 158.8 +/- 26 g, respectively) but a lower hyperemic response (73.3 +/- 2 and 102.3 +/- 10 percent, respectively). These data suggest that severe left ventricular hypertrophy is associated with a reduction in coronary vascular reserve; it is speculated that this decrease in the vascular reserve capacity may be related to the ischemic component of hypertrophic heart disease.     

左心室中部肥厚型梗阻性心肌病临床及造影特征分析

目的 分析左心室中部肥厚型梗阻性心肌病患者的临床及心血管造影特征.方法 5例(男:女=3:2)临床诊断为左心室中部肥厚型梗阻性心肌病的患者,年龄16～73(44±22)岁.所有患者均接受左心导管及心血管造影检查,并记录左心室心尖部-左心室基底部-左心室流出道-升主动脉连续压力.结果 5例患者中胸闷气短者4例,其中2例合并晕厥.所有患者心前区均可闻及收缩期杂音,且均存在左心室壁肥厚,室间隔厚度为19～31(23.8±5.4)mm,左心室舒张末期横径为35～55(43.4±7.4)mm,左心室射血分数为53%～70%、平均为(64.2±6.9)%.5例患者均存在左心室高电压伴异常Q波,其中1例患者合并阵发性室性心动过速,另有1例患者合并完全性左束支传导阻滞.左心导管检查证实收缩期左心室中部均存在梗阻,其中1例患者同时合并左心室流出道梗阻.左心室中部收缩期压力阶差为45～102(68.6±24.1)mm Hg(1 mm Hg=0.133 kPa).心血管造影检查提示前降支中段肌桥1例,冠状动脉粥样硬化性心脏病1例.另外,2例患者合并左心室心尖部室壁瘤.结论 左心室中部肥厚型梗阻性心肌病的临床特征不同于其他类型的肥厚型心肌病,完善的左心导管检查及造影有利于诊断并指导临床治疗.     

Left ventricular hypertrophy secondary to systemic hypertension: its effect on coronary hemodynamics]

To clarify the characteristics and possible causes of phasic blood velocity patterns in pressure overload hypertrophy, we measured blood flow velocities in the left anterior descending coronary arteries in 16 patients with left ventricular hypertrophy secondary to systemic hypertension. These measurements were made with a 20MHz Doppler catheter. All patients had normal coronary arteriograms. The blood flow velocity patterns were characterized by the decrease in the rise of early diastolic inflow velocity. Prolongation in the time from the onset of diastole to peak velocity (TDPV) correlated with the degree of left ventricular hypertrophy. TDPV was prolonged in proportion to the increase in the peak left ventricular systolic pressure and left ventricular ejection fraction. The flow reserve calculated from the ratio of the diastolic mean velocity after the intracoronary injection of papaverine to the resting flow showed a trend toward the decrease proportional to the prolongation in TDPV due to an increase of wall thickness. In conclusion, preceding systolic vascular compression and systolic vascular strain can be factors causing early diastolic inflow disturbance in left ventricular hypertrophy secondary to hypertension. The decrease of coronary reserve may partially be attributable to the decrease in the rise of early diastolic inflow velocity.     

Immediate effect of aortic valve replacement for aortic stenosis on left ventricular diastolic chamber stiffness.

Diastolic dysfunction is common after coronary artery bypass surgery, and we hypothesized that left ventricular (LV) hypertrophy associated with aortic stenosis may lead to worsening LV diastolic function after aortic valve replacement for aortic stenosis. Transesophageal echocardiographic LV images and simultaneous pulmonary arterial wedge pressures were used to define the LV diastolic pressure cross-sectional area relation before and immediately after aortic valve replacement for aortic stenosis in 14 patients. In all patients, LV diastolic chamber stiffness increased, as evidenced by a leftward shift in the LV diastolic pressure cross-sectional area relation. At comparable LV filling (pulmonary arterial wedge) pressures the mean LV end-diastolic cross-sectional area preoperatively was 17.9 +/- 1.7 cm2, but decreased by 32% after aortic valve replacement to 12.1 +/- 1.2 cm2 (p = 0.0001). In conclusion, after aortic valve replacement, diastolic chamber stiffness increased in all patients.     

Muscular subaortic stenosis

A boy one year of age presented the features of aortic stenosis with a systolic gradient of 40 mm. Hg across the aortic valve. At surgery with the chest open a systolic gradient of 35 mm. Hg was measured across the pulmonic valve. No operable lesion was found. The child died postoperatively.

Autopsy revealed striking ventricular hypertrophy and a ring of muscular hypertrophy obstructing the outflow of the left ventricle. The right ventricle was normally formed. The suggested diagnosis was congenital idiopathic hypertrophy and its relation to asymmetric hypertrophy was raised.

Similar reported cases are reviewed. The difficulty and importance of differentiating muscular subaortic stenosis from congenital aortic and subaortic stenosis are stressed.     

The myocardial supply:demand ratio--a critical review.

Myocardial ischemia occurs when there is an imbalance between myocardial oxygen demand and supply, and it is usually entirely or predominantly subendocardial. Animal experiments have shown that relative subendocardial ischemia (a reduced inner:outer flow ratio) can be predicted quite accurately from the ratio of two pressure-time areas:DPTI, the area between diastolic aortic and left ventricular pressures, and SPTI, the area beneath the systolic left ventricular pressure curve. Although the importance of relating supply and demand is obvious, care is needed in applying the results of these animal experiments to man. Recent work has shown that the critical DPTI:SPTI ratio below which subendocardial ischemia occurs is about 0.4 to 0.5 rather than 0.7 to 0.8, as originally reported. On the other hand, the critical ratio may be raised to an unknown extent by myocardial edema or hypertrophy, or by thickened or narrowed coronary arteries. Furthermore, the critical ratio is not independent of absolute coronary diastolic pressure: It is much lower than 0.4 when coronary pressures are high, perhaps because intramyocardial diastolic pressures are much higher than once thought. Further work is required to allow an important physiologic concept to be used in making decisions about patients with heart disease.     

Study of the relaxation phase of the right ventricle]

The purpose of our study was to investigate the existence or not of an isovolumic relaxation period in the right ventricle in experimental animals with normal pressures in the pulmonary artery. Right and left ventricular pressures, pulmonary and aortic pressures (microtransducers), pulmonary flow, ventricular diameters (sonomicrometer), were recorded at the same time, in 10 sheep anesthetized intravenously with pentobarbital. We obtained "off line" the first ventricular pressures derivative, the ventricular volumes and the pressure-volume loops of both ventricles. The minimum systolic right ventricular volume coincided with 0 pulmonary flow, and both with a diastolic pressure value of 0-5 mmHg in that ventricle. Once the minimum systolic volume was reached, a rapid increase of the right ventricular volume started. The right ventricular pressure-volume loop, unlike the left ventricular one, adopted a non-rectangular shape. The right ventricular ejection period lasted until the beginning of the next filling phase. We concluded that there is no right ventricular isovolumic relaxation period.