Adrenergic coronary vasoconstriction helps maintain uniform transmural blood flow distribution during exercise

The hypothesis that alpha-adrenergic coronary vasoconstriction helps maintain a uniform transmural distribution of myocardial blood flow during exercise was tested in dogs. Carotid artery loops were surgically constructed and a splenectomy performed three weeks prior to study. On the day of study, the dog was anesthetized briefly (fentanyl and nitrous oxide) for percutaneous catheterization, and alpha-receptors in one myocardial region were blocked with phenoxybenzamine (0.25 mg/kg) infused selectively into the left circumflex coronary artery. Recirculation of phenoxybenzamine was minimized by drainage of coronary sinus outflow during the infusion. After the dog recovered from the anesthesia, regional blood flow was measured at rest and during graded treadmill exercise with the microsphere technique calibrated by reference blood samples. Average transmural flow was limited by alpha-vasoconstriction and was less in the region where alpha-receptors were intact than in the region where they were blocked, as has been described by others. The ratio of inner layer myocardial blood flow to outer layer flow was better maintained in the region with alpha-receptors intact than in the region with alpha-receptors blocked when myocardial oxygen consumption was 150 microliter/min/g or greater (p less than 0.001). Even though average transmural flow was limited by alpha-receptor activation, inner layer myocardial blood flow was greater in the region with alpha-receptors intact than in the region with alpha-receptors blocked when myocardial oxygen consumption was 500 microliter/min/g or more (p less than 0.05). In conclusion, adrenergic coronary vasoconstriction mediated by alpha-receptors helps to maintain a uniform transmural distribution of myocardial blood flow during exercise in spite of limiting average transmural flow.     

Adrenergic nervous system and left ventricular mass in primary hypertension

A link between the activity of the adrenergic nervous system and left ventricular hypertrophy has frequently been found in hypertensives. In 16 patients with untreated primary hypertension of mild to moderate degree, we have evaluated the possible correlations between echocardiographic left ventricular mass (LVMe) and sympathetic nervous system activity, using pressor response to exogenous noradrenaline infusion, measurement of 24-h catecholamine urinary excretion and pressure response to ergometric exercise. Pressor response to noradrenaline infusion was significantly related to echocardiographic measures of left ventricular hypertrophy (correlation coefficients were: -0.60 for LVMe; -0.51 for septal thickness (ST); -0.51 for posterior wall thickness). Left ventricular mass was also related to systolic blood pressure measured during ergometric exercise (correlation coefficients were: 0.52 with LVM index, 0.51 with LVMe and 0.61 with ST). Arterial wall hypertrophy has been identified as being responsible for the vascular hyperreactivity in hypertension. A likely explanation of our findings is that the degree of left ventricular hypertrophy is associated with the degree of structural alterations of the resistance vessels and that the vascular impairment is responsible for the increased pressure response to noradrenaline.     

Assessment of right ventricular afterload by pressure waveform analysis in acute pulmonary hypertension

AIM: To characterize hydraulic right ventricle (RV) af- terload by pulmonary arterial pressure waveform analy- sis in an acute pulmonary hypertension (PH) model. METHODS: Pulmonary artery (PA) flow and pressure were recorded in six anesthetized sheep. Acute iso- baric PH was induced by phenylephrine (active) and PA mechanical constriction (passive). We estimated the amplitude of the forward and reflected pressure waves according to the inflection point. In most cases the in- flection pressure was smooth, thus the inflection point was defined as the time at which the first derivative ofpulmonary arterial pressure reached its first minimum. We calculated the input and characteristic (Z C , time- domain Li method) impedances, the capacitance index (stroke volume/pulse pressure), the augmentation index (AI) (reflected pressure/pulse pressure), the frac- tional pulse pressure (pulse pressure/mean pressure) and the wasted energy generated by the RV due to wave reflection during ejection (E W ). RESULTS: Pulse pressure, fractional pulse pressure, AI and Z C increased and capacitance index decreased during passive PH with respect to control (P < 0.05). In contrast, Z C and the capacitance index did not change and E W and the AI decreased during active PH. Pulse pressure correlated with E W and Z C and the AI was cor- related with E W (r > 0.6, P < 0.05). CONCLUSION: PA pressure waveform analysis al- lows the quantification of the dynamic RV afterload. Prospective clinical studies will be necessary to validate this time-domain approach to evaluate the dynamic RV afterload in chronic PH.     

Changes in right ventricular ejection fraction in right coronary angioplasty

In order to analyse the response of the right ventricule (RV) to transient myocardial ischaemia, the RV ejection fraction was measured using a new rapid response thermodilution catheter in 15 patients (14 men and 1 woman: average age 58 +/- 7 years) referred for percutaneous transluminal coronary angioplasty of a dominant right coronary artery. Only patients with single vessel disease with a proximal stenosis of the right coronary without a visible collateral circulation who had no previous history of myocardial infarction were included. Right heart catheterisation was performed with a rapid-response thermodilution catheter which enabled measurement of heart rate, cardiac index, RV end-diastolic and end-systolic volumes and RV ejection fraction. Angioplasty was carried out with the usual steerable balloon catheters. During balloon inflation, there was a slight increase in RV end-diastolic volume (from 78 +/- 11 ml/m2 to 85 +/- 13 ml/m2 at 60 seconds; p less than 0.01) and a large increase in RV end-systolic volume (from 29 +/- 8 ml/m2 to 35 +/- 8 ml/m2 at 30 seconds and 43 +/- 11 ml/m2 at 60 seconds, p less than 0.001) leading to a significant decrease in RV ejection fraction (from 62 +/- 8% to 56 +/- 6% at 30 seconds and 51 +/- 7% at 60 seconds; p less than 0.001). All parameters returned to basal values two minutes after the dilatation. Acute occlusion of the proximal segment of the right coronary artery is therefore associated with a marked change in right ventricular function which rapidly returns to normal after the coronary circulation is restored.     

Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty: The only true 'model' to study ECG changes in acute, isolated right ventricular infarction

An isolated right ventricular infarction occurs rarely and dataon its electrocardiographic appearance and underlying angiographicallyproven cause are scarce. The electrocardiographic response ofacute right ventricular ischaemia is often obscured by the coexistingforces of the ischaemic mass of the inferior wall of the leftventricle when the right coronary artery itself becomes occluded.Percutaneous transluminal coronary angioplasty of the rightcoronary artery may cause an isolated occlusion of a right ventricularbranch. We encountered this phenomenon in nine patients. Inall, it led to acute isolated right ventricular ischaemia withST elevations in the right precordial leads (V₁–V₃, V₃Rand V₄R on the electrocardiogram. We conclude that the ECG pattern of pure right ventricular ischaemiacan be seen when an isolated occlusion of a large right ventricularbranch occurs, for example as a complication of percutaneoustranslummal coronary angioplasty.     

Right ventricular subendocardial infarction in a patient with pulmonary hypertension,right ventricular hypertrophy,and normal coronary arteries

Right ventricular infarction is usually associated with coronary artery disease and concomitant left ventricular infarction. Isolated right ventricular subendocardial necrosis was discovered at autopsy in a 52-year-old woman with pulmonary hypertension, right ventricular hypertrophy, and normal coronary arteries, who died with septicemia 41 days after mitral valve replacement. This represents the first well-documented report of isolated right ventricular subendocardial infarction associated with normal coronary arteries.     

Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction.

BACKGROUND: A normally contracting right ventricular apex associated to a severe hypokinesia of the mid-free wall ('McConnell sign') has been considered a distinct echocardiographic pattern of acute pulmonary embolism. OBJECTIVE: To evaluate the clinical utility of the 'McConnell sign' in the bedside diagnostic work-up of patients presenting to the Emergency Department with an acute right ventricular dysfunction due to pulmonary embolism or right ventricular infarction. DESIGN: Among 201 patients, consecutively selected from our clinical database and diagnosed as having massive or submassive pulmonary embolism or right ventricular infarction, 161 were suitable for an echocardiographic review of regional right ventricular contraction and were included in the study. There were 107 cases with pulmonary embolism (group 1) and 54 cases with right ventricular infarction (group 2). All echocardiographic studies were randomly examined by two experienced and independent echocardiographers, blinded to the patient diagnosis and without Doppler informations. RESULTS: The McConnell sign was detected in 75 of 107 patients in group 1 (70%) and in 36 of 54 patients in group 2 (67%); the finding was absent in 32 cases in group 1 and in 18 cases in group 2 (P=0.657). The sensitivity, specificity, positive and negative predictive values of the McConnell sign for the diagnosis of pulmonary embolism were respectively 70, 33, 67 and 36%. CONCLUSIONS: In a clinical setting of patients with acute right ventricular dysfunction the McConnell sign cannot be considered a specific marker of pulmonary embolism.     

Pulmonary hemodynamics and right ventricular function in hypertension

Pulmonary and systemic hemodynamics in 16 hypertensive subjects (group I) with left ventricular (LV) hypertrophy (ECG and echo criteria) and in 17 hypertensive subjects with ECG signs of LV strain (group II), were compared with those in 14 normal individuals. An augmented pulmonary arteriolar resistance (PAR) in group I and to a larger extent in group II accounted for the pulmonary pressure elevation in both groups. Increase in PAR was unrelated to pulmonary blood flow and volume, pleural pressure, arterial PO2, PCO2 and pH, and could not be explained entirely by the left ventricular end-diastolic pressure changes. In group I, left (L.MSEJR) and right (R;MSEJR) mean systolic ejection rate, stroke index (SI) and mean velocity of circumferential fiber shortening (VCF) were enhanced in spite of the heightened pressure load on both sides of the heart. In group II, a large reduction of SI, L.MS.EJR, R.MSEJR and VCF, as well as the relationship between ventricular filling pressures and SI, documented a compromised performance of both ventricles, Findings indicate that: systemic hypertension is associated with elevation of pulmonary arterial pressure and of PAR which is not necessarily a consequence of impairment in LV function; LV hypertrophy is associated with enhanced performance of either ventricle; in coincidence with development of ECG signs of LV strain, the performance of both sides of the heart deteriorates. A functional interdependence of the two ventricles is suggested.     

Arrhythmogenic right ventricular cardiomyopathy with left ventricular involvement mimicking acute coronary syndrome - two case reports

We describe 2 patients with arrhythmogenic right ventricular cardiomyopathy (ARVD): 58 year-old female and 48 year-old man. Both patients presented with echocardiographic features typical for ARVD and impaired systolic left ventricular function. Both patients had symptoms resembling acute coronary syndrome and received cardioverter-defibrillator due to recurrent sustained ventricular tachycardia.     

Alterations in left ventricular three-dimensional dynamic geometry and systolic function during acute right ventricular hypertension in the conscious dog

Fifteen chronically instrumented, conscious dogs were studied to determine whether, in the intact circulation, mechanical interactions dictated by the anatomic contiguity of the two ventricles significantly alter left ventricular (LV) dynamic geometry and systolic function during acute right ventricular (RV) hypertension. The three-dimensional geometry of the left ventricle was monitored with three pairs of ultrasonic dimension transducers; ventricular pressures were measured with micromanometers. Data collected during pulmonary artery constriction (RV pressure 68 +/- 8/7 +/- 4 mm Hg) were compared with control data collected at matched heart rates (RV pressure 32 +/- 8/4 +/- 4 mm Hg). During pulmonary artery constriction, mean calculated LV end-diastolic volumes decreased from 69.2 +/- 20.0 to 56.2 +/- 21.3 cm3 (p less than or equal to 0.05). Mean systolic stroke volume decreased from 20.6 +/- 5.5 to 14.0 +/- 6.3 cm3 (p less than or equal to 0.05). These changes were entirely accounted for by alterations in the behavior of the LV septal-free wall minor axis and rearrangements in LV equatorial geometry. When the pulmonary artery was constricted, elongation of the septal-free wall axis occurred during isovolumic systole and was accompanied by a reciprocal decrease in anterior-posterior dimension. Most of the decrease in septal-free wall dimension occurred during relaxation and early diastole rather than during ejection. Mean septal-free wall end-diastolic dimension decreased from 5.45 +/- 0.69 to 4.90 +/- 0.75 cm (p less than or equal to 0.05). The mean systolic decrease in septal-free wall dimension fell from 0.36 +/- 0.18 to 0.14 +/- 0.22 cm (p less than or equal to 0.05). The end-diastolic dimensions and systolic shortening of the LV anterior-posterior minor axis and base-apex major axis were not significantly altered by pulmonary artery constriction. These findings suggest that during acute RV hypertension, impairment of LV systolic function and rearrangements in LV dynamic geometry are primarily the result of the anatomic contiguity of the two ventricles.     

Myocardial bridging confined to the right ventricular branch of the right coronary artery in a patient with severe pulmonary hypertension

Although myocardial bridges are mostly confined to the left anterior descending coronary artery, several cases of right coronary artery myocardial bridging have been reported in the literature. In the current case report, we present a 65-year-old female with a well-functioning mechanical mitral valve prosthesis, severe pulmonary hypertension and right ventricle wall motion abnormality in whom diagnostic angiography revealed myocardial bridging confined to the right ventricular branch of the right coronary artery.     

Effects of acute right ventricular systolic hypertension on regional myocardial blood flow in anesthetized dogs

An important determinant of right ventricular (RV) myocardial blood flow is coronary driving pressure (CDP)—the pressure difference between RV and aorta. Since right ventricular systolic hypertension (RVSH) decreases RV CDP, it might limit blood flow to RV muscle. To study this we constricted the pulmonary artery in openchest dogs to give RV to aortic systolic pressure ratios of 0.25 to 0.40 (mild RVSH) and over 0.40 (moderate RVSH). We measured regional myocardial blood flow with 8 to 10 μ diameter radioactive microspheres, RV CDP by integrating the aortic-RV pressure difference per minute (pressure index—PI), and assessed myocardial oxygen needs of each ventricle from its tensiontime index (TTI).Flow to RV wall rose with mild and fell with moderate RVSH; differences were not significant. The ratio of RV myocardial flow to TTI remained normal with mild RVSH but fell 50 per cent with moderate RVSH. The ratio of RV PI to TTI was 10.3 ± 2.7 (mean and standard deviation) in controls, 5.6 ± 1.4 in mild RVSH, 2.4 ± 1.0 in moderate RVSH, and 1.8 ± 0.6 with acute heart failure.Reducing RV PI initially causes coronary vasodilatation. After maximal vasodilatation, further reduction decreases flow relative to oxygen needs. Underperfusion of RV myocardium may be predicted from information derived from RV and aortic pressure tracings.     

Right ventricular coronary flow in arterial hypertension

Right ventricular (RV) coronary circulation in systemic hypertension offers an opportunity to assess the effects of marked increases in coronary perfusion pressure in vivo without appreciable increases in workload or marked hypertrophy of the cardiac chamber. This study investigates RV coronary circulation in renal hypertensive rats (RHR). Mean arterial pressure rose by 50% to 60% in RHR as compared to control groups and RV mass increased by 15% (7.15 vs 6.19 mg/gm body weight, p less than 0.01). Coronary blood flow, which was measured by left atrial injection of microspheres in conscious rats, was not significantly different between study groups both at rest and after maximal coronary vasodilation with carbochrome (6 mg/kg). However, minimal RV coronary resistance level per gram were significantly elevated (p less than 0.05) in RHR. A second study was designed to further dissociate the effects of arterial hypertension from the effects of changes in RV mass in RHR. In one group, blood pressure was acutely reduced by 1 week of captopril therapy, while RV mass remained high. In the second group, captopril was discontinued after 14 weeks of treatment, allowing arterial pressure to rise, while RV mass, which had regressed with treatment, remained normal. After treatment, RV minimal coronary resistance levels remained high in the short-term-treated hypertensive rats, but returned to normal levels in the long-term-treated RHR. These results suggest the following possibilities: the RV is not immune to the effects of systemic hypertension, coronary structural changes are probably the main factor that accounts for the increase in RV coronary resistance levels, and coronary alterations are amenable to long-term antihypertensive therapy.     

肺动脉高压患者右室机械活动延迟与右室收缩功能的相关性研究

目的探讨肺动脉高压患者右室机械活动延迟与右室收缩功能之间的关系。方法51例肺动脉高压患者按肺动脉高压程度分为轻、中、重3组,并选取30名健康人为对照组,采用定量组织多普勒技术（QTVI）取心尖四腔切面分别测量右室三尖瓣环、室间隔三尖瓣环收缩期达峰时间,二者差值为右室机械收缩延迟时间（RV—IVSd）;常规二维超声同一切面测量右室舒张末期面积、收缩末期面积,计算出右室面积变化分数（RVa％）。结果（1）与对照组比较,轻、中、重度肺动脉高压组RV-IVSd明显延迟（P〈0．05）,且肺动脉压力越高,延迟越明显;（2）轻度组RVa％与对照组间差异无统计学意义（P〉0．05）,而中、重度组RVa％低于对照组（P〈0．05）;（3）肺动脉高压各组RV—IVSd与RVa％相关性均良好（r=-0．79;r=-0．66;r=-0．80）。结论RV—IVSd可在一定程度上反映右心收缩功能,为超声评估右室收缩功能提供了一种新指标。