Left ventricular pressure-volume relations shift to the left after long-term loss of pericardial restraint

The short-term effect of pericardiectomy is to shift the in vivo left ventricular (LV) pressure-volume curve to the right. We studied nine weight-matched pairs of male guinea pigs 28 to 39 days (mean 35) after complete pericardiectomy or sham thoracotomy to determine the long-term effects of pericardiectomy on LV pressure-volume relations. Hemodynamic and in vitro LV pressure-volume data were collected in matched pairs on the same day, 2 to 3 hr after catheter placement and recovery from anesthesia. Cardiac output was measured by the microsphere reference sample method. Postsurgical weight gain was similar in both groups: 823 +/- 6 (mean +/- SD) to 925 +/- 6 g in the pericardiectomy group and 829 +/- 7 to 927 +/- 7 g in the sham thoracotomy group. We found no difference in LV weight: 1.555 +/- 0.145 g in the pericardiectomy group vs 1.564 +/- 0.148 g in the sham thoracotomy group, nor any difference in heart rate, mean arterial, right atrial, or left ventricular end-diastolic pressures, cardiac outputs, or stroke volumes (p = NS). LV pressure-volume relations, however, were shifted to the left in the pericardiectomy group (p less than .005). At 10 mm Hg, LV volume in the pericardiectomy group (0.85 +/- 0.22 cc) was less than that in the sham thoracotomy group (1.02 +/- 0.15 cc; p less than .025). The LV stress-elastic modulus relationship was not different between groups (p greater than .30). One month after pericardiectomy, LV pressure-volume relations in vitro were shifted to the left without a change in LV weight, LV elastic modulus, or hemodynamics. We speculate that this shift compensates for the lack of pericardial restraint and returns LV volume and hemodynamics to normal in vivo.     

Changes in left ventricular internal diameter with increasing pericardial pressure.

Changes in left ventricular internal diameter resulting from increasing intrapericardial pressure induced by increasing the pericardial fluid volume were studied in closed chest, anaesthetized dogs. Left ventricular internal diameters were measured by placing an ultrasonic dimension catheter in the left ventricle at the time of the experiments. With increasing pericardial pressure, significant increases occurred in heart rate and mean left atrial pressure. Left ventricular end-diastolic and end-systolic diameter progressively decreased as the pericardial pressure was elevated. After beta adrenergic blockade with propranolol (1 mg/kg), the decline in end-systolic diameter during pericardial tamponade was significantly reduced. These observations indicate the importance of the systolic reserve and the role of beta adrenergic receptors in the adaptation of the left ventricle to increases in pericardial tamponade.     

Exercise blood pressure response is related to left ventricular mass

An exaggerated SBP response to exercise has been associated with increased left ventricular (LV) mass in some but not all studies. A total of 43 women and 34 men, aged 55-75 years, without evidence of cardiovascular disease, with a mean resting BP of 142+/-9/77+/-8 mmHg had their BP measured at rest and during maximal treadmill exercise. LV mass was measured using magnetic resonance imaging. LV mass was adjusted for lean body mass, which was assessed by dual energy X-ray absorptiometry. LV mass was within the normal range for the majority of the subjects. Among the resting and exercise BP indices, maximal SBP was the strongest correlate of LV mass (r=0.41, P<0.05). In multivariate analysis, maximal SBP was independently associated with LV mass after adjustment for lean body mass and gender, explaining 3% of the variance (P<0.05). Maximal exercise SBP is a modest but still independent predictor of LV mass in older persons with normal LV mass. These results raise the possibility that the SBP response to maximal exercise is an early marker of LV hypertrophy.     

Multiple bilateral coronary-biventricular fistulas with elevated left ventricular end-diastolic pressure

Arterioventricular fistulas are relatively rare abnormalities and the etiology may be congenital or traumatic. We report a case of a 51-year-old woman in which all three coronary arteries emptied into both ventricles via multiple small fistulas resulting in elevated left ventricular end-diastolic pressure.     

Operating characteristics of the Finapress system to predict elevated left ventricular filling pressure

BACKGROUND: Dyspnea is a common symptom and can be caused by many different conditions. The detection of congestive heart failure (CHF) is sometimes difficult. HYPOTHESIS: The pulse amplitude ratio (PAR) measured by the Finapress procedure during a Valsalva maneuver can detect elevated left ventricular end-diastolic pressure (LVEDP) accurately over a wide range of values. METHODS: Comparison of the estimated LVEDP by PAR with the invasively measured LVEDP before and after ventriculography during coronography was made in 101 consecutive stable patients referred for chest pain and/or chronic dyspnea. RESULTS: A significant correlation was found between the catheter-measured LVEDP (range 3-40 mmHg) and the PAR (R2 = 0.70, p < 0.001). The receiver operator characteristics (ROC) of the PAR to detect an LVEDP > 15 mmHg can be considered to be excellent, with an area under the ROC curve achieving 0.92 (95% confidence interval [CI] 0.87-0.96; p < 0.001). A PAR of > 0.675 predicted the presence of an LVEDP > 15 mmHg with a sensitivity of 0.865 (95% CI 0.780-0.926) and a specificity of 0.847 (95% CI 0.730-0.928). The positive and negative LRs were 5.70 and 0.16, respectively. CONCLUSIONS: The observed likelihood ratios confirm that the PAR determined by the Finapress procedure may be a useful bedside diagnostic tool in patients with cardiac conditions.     

Independence of changes in left ventricular diastolic properties of pericardial pressure.

There has been much interest in the published reports as to the extent to which measured left ventricular diastolic properties are affected by the pericardium. In this study observations were made on 24 patients, seven days after cardiopulmonary bypass. Left ventricular dimensions were measured from echocardiographic recordings and left ventricular diastolic pressure assessed from measurements of isovolumic relaxation time. Pericardial pressure was measured directly using a small solid state transducer inserted into the pericardial space at the time of operation. Left ventricular diastolic properties were altered by either isometric handgrip or glyceryl trinitrate administration. Isometric handgrip produced an increase in cavity dimension at end-systole and diastole, with reduction in isovolumic relaxation time, suggesting an increase in left ventricular end-diastolic pressure; glyceryl trinitrate produced the reverse effect, with decreased cavity dimensions and prolongation of isovolumic relaxation time. These changes occurred in the absence of significant changes in pericardial pressure. We therefore conclude that even in the rather unusual conditions of the early postoperative period, when the sensitivity of pericardial pressure to small volume changes might be expected to be increased, substantial changes in left ventricular diastolic properties can occur without detectable alteration in pericardial pressure.     

Ratio of left atrial to left ventricular size: an anatomical marker of the diastolic left ventricular pressure-volume relationship

BACKGROUND: Classification of diastolic heart function is best defined by the degree of leftward and upward shift of the diastolic pressure-volume relationship (DPVR). Direct measurement of DPVR, however, requires invasive techniques. Increased left atrial (LA) size is a marker of left ventricular (LV) diastolic hypertension, and so, the LA/LV diameter ratio has the potential to mark the degree of upward and leftward shift in the LV-DPVR. We thus investigated the association of this novel marker with exposures known to induce diastolic dysfunction and with clinical evidence of diastolic dysfunction. METHODS AND RESULTS: Reports from 7,803 patients undergoing maximal exercise stress echocardiography were reviewed. Increased LA/LV diameter ratio predicted diminished exercise capacity (P < 0.001) in a multivariate regression analysis. Increased LA and decreased LV diameters were each independently associated with exercise capacity (P < 0.001, both). Increased LA/LV diameter ratio was associated with hypertension (P = 0.001), diabetes (P = 0.03) and with increased severity of LV hypertrophy (P< 0.001). Those with LA/LV diameter ratio > or = 1.0 were more likely to use loop diuretics, odds ratio = 2.5 [95% CI, 1.4, 4.5], compared to those with lower ratio values. CONCLUSIONS: Increased LA/LV diameter ratio was observed in subjects with hypertension, diabetes and LV hypertrophy. Increased ratio predicted worse exercise capacity and was associated with more frequent loop diuretic use. These data are consistent with the hypothesis that this ratio is a noninvasive marker of the LV-DPVR.     

The use of left ventricular end-ejection pressure and peak pressure in the estimation of the end-systolic pressure-volume relationship

The end-systolic pressure-volume relationship (ESPVR) as derived from left ventricular pressure-volume loops has gained increasing acceptance as an index of ventricular contractile function. In animal experiments the ESPVR has been defined as a line connecting the upper left corners of several differently loaded pressure-volume (P-V) loops with a slope parameter Ees and a volume axis intercept parameter Vo. In the clinical setting, several variants of the ESPVR have been determined with use of peak left ventricular pressure, end-ejection pressure, and end-ejection volume. The maximum P-V ratio has also frequently been measured. We attempted to determine which of these alternatives resulted in good approximations of the reference ESPVR in eight isolated canine ventricles that ejected into a simulated arterial impedance system with resistance, compliance, and characteristic impedance. We determined various versions of the ESPVR from the same set of beats quickly obtained with little change in inotropic background. To vary ventricular pressure wave forms, each of the arterial impedance parameters was independently controlled at 50%, 100%, and 200% of normal. Against each of the nine combinations of the impedance parameters four P-V loops were obtained under four preloads and from each of the sets of four P-V loops, the reference ESPVR, linear regression of the peak pressure on end-ejection volume (ESPVRPP-EEV), and linear regression of end-ejection pressure on end-ejection volume (ESPVREEPV) were determined. In addition, the maximum P-V ratio (MPVR) was calculated for each P-V loop.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right ventricular pressure elevated in one-kidney,one clip Goldblatt hypertensive rats

Both renal and respiratory diseases are common with high mortality rate around the world. This study was the first to compare effects of two kidneys, one clip (2K1C) and one-kidney, one clip (1K1C) Goldblatt hypertension on right ventricular pressure during normal condition and mechanical ventilation with hypoxia gas. Male Sprague–Dawley rats were subjected to control, 2K1C, or 1K1C groups. Twenty-eight days after the first surgery, animals were anesthetized, and femoral artery and vein, and right ventricle cannulated. Systemic arterial pressure and right ventricular systolic pressures (RVSP) were recorded during ventilation the animals with normoxic or hypoxic gas. RVSP in the 1K1C group was significantly more than the control and 2K1C groups during baseline conditions and ventilation the animals with hypoxic gas. Administration of antioxidant Trolox increased RVSP in the 1K1C and control groups compared with their baselines. Furthermore, there was no alteration in RVSP during hypoxia in the presence of Trolox. This study indicated that RVSP only increased after 28 days induction of 1K1C but not 2K1C model. In addition, it seems that the response to hypoxic gas and antioxidants in 1K1C is more than 2K1C. These data also suggest that effects of 1K1C may partially be related to reactive oxygen species (ROS) pathways.     

The pressure-volume relation and the mechanics of left ventricular contraction

The left ventricle is represented as an elastic thick-walled cylinder contracting symmetrically. The force generated by the active state of the myocardium in the radial direction is represented by body force (force/unit volume) and is included in the mathematical formalism that describes the contraction of the left ventricle. An equation for the P-V relation in the left ventricle is derived and various applications to study cardiac mechanics are discussed. The results obtained tend to demonstrate that the active force generated by the myocardium during an ejecting contraction reaches its maximum value near the end of the systolic phase, when the slope E of the P-V line reaches its maximum value Em, and that it is related to the peak isovolumic pressure.     

Relationship between blood pressure response during exercise and tendency to left ventricular hypertrophy

From among subjects who were examined by submaximal exercise testing in 1987, 54 were selected in order to examine the relationship between the blood pressure response during exercise and the tendency to develop left ventricular hypertrophy. Only those subjects having resting systolic blood pressure values between 120 mmHg and 140 mmHg were selected. The maximum systolic blood pressure during submaximal exercise was highly correlated with the sum of the R wave amplitude in V5 and the S wave amplitude in V1 of the resting ECG (r = 0.496, p less than 0.001, n = 54), as well as with the left ventricular mass normalized for body surface area (r = 0.609, p less than 0.005, n = 23). The maximum systolic blood pressure measured during submaximal exercise did not correlate with age or exercise duration. These results suggest that a greater blood pressure response during exercise is related to the tendency to develop left ventricular hypertrophy.     

Right and left ventricular function and pulmonary artery pressure in patients with bronchiectasis

BACKGROUND: Bronchiectasis may have deleterious effects on cardiac function secondary to pulmonary hypertension (PH). This study was designed to assess cardiac function and determine the prevalence of PH in patients with cystic and cylindrical bronchiectasis. METHODS: A cross-sectional study of patients with bronchiectasis diagnosed by CT scan was conducted at King Khalid University Hospital, Riyadh, Saudi Arabia between December 2005 and January 2007. Pulmonary function tests were performed, arterial blood gas measurements were made, and cardiac function and systolic pulmonary artery pressure (SPAP) were assessed by echocardiography. RESULTS: Of 94 patients (31% men, n = 29), 62 patients (66%) had cystic bronchiectasis and 32 patients (34%) had cylindrical bronchiectasis. Right ventricular (RV) systolic dysfunction was observed in 12 patients (12.8%), left ventricular (LV) systolic dysfunction was observed in 3 patients (3.3%), and LV diastolic dysfunction was observed in 11 patients (11.7%); all had cystic bronchiectasis. RV dimensions were significantly greater in the cystic bronchiectasis group, and were positively correlated with SPAP (p < 0.0001) and negatively correlated with Pao2 (p < 0.016). Other hemodynamic variables were not different between groups. PH in 31 patients (32.9%) was significantly greater in patients with cystic bronchiectasis compared with cylindrical bronchiectasis (p = 0.04). In cystic bronchiectasis, SPAP was positively correlated with Paco2 (p = 0.001), and inversely correlated with Pao2 (p = 0.03), diffusion capacity of the lung for carbon monoxide percentage (p = 0.02), and FEV1 (p = 0.02). CONCLUSIONS: RV systolic dysfunction and PH were more common than LV systolic dysfunction in bronchiectatic patients. LV diastolic dysfunction was mainly seen in severe PH. We recommend detailed assessment of cardiac function, particularly LV diastolic function, in patients with bronchiectasis.     

Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.

Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 +/- 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a,a') derived from P-V and normalized P-V relations, respectively, for end-diastolic myocardial elastic stiffness (ES or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (KS or KE) of the circumferential stress-strain relation. Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 +/- 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV,dP/dV/V,ES and EE and a tendency for increase in the chamber stiffness constants (a,a') and myocardial stiffness constants (KS, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid- and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.     

Human left ventricular end-systolic pressure-volume relationship in a cylinder model

The relationship between myocardial total force and length at the end of systole appears to be linear, and the slope of this relationship is considered to be an appropriate index of myocardial contractile state, independent of preload and afterload. However, direct measurements of this relation may be impossible in the intact human heart, and thus, alternative indices such as the left ventricular end-systolic stress-length, stress-strain, pressure-volume, and pressure-dimension slopes have been proposed to evaluate myocardial contractility in the intact heart. However, the mathematical relationship between the myocardial end-systolic total force-length relation and any of these left ventricular end-systolic relations remains unclear. In this study, assuming a linear myocardial end-systolic total force-length relation in an intact ventricle, we obtained mathematical formulae for the left ventricular end-systolic stress-strain, pressure-radius, and pressure-volume relations, using a cylinder model of the left ventricle. The results obtained using these formulae and the cylinder model were found to match accurately findings obtained from earlier experimental and clinical studies of these left ventricular end-systolic relations. Thus, this model could mathematically account for the relationships between the slopes of the myocardial end-systolic total force-length relation and these left ventricular end-systolic relations.