Modification of cardiac function in cirrhotic patients with and without ascites

OBJECTIVES: Abnormalities in cardiac function have been reported in liver cirrhosis, suggesting a latent cardiomyopathy in these patients. In this study we investigated cardiac function in cirrhotic patients and in controls. METHODS: A total of 20 cirrhotic patients without previous or ongoing ascites, 20 cirrhotic patients with moderate-to-severe ascites, and 10 healthy controls were studied by two-dimensional Doppler echocardiography. Cardiac dimensions and left and right ventricular function were evaluated. The left ventricular geometric pattern was calculated according to Ganau's criteria. Diastolic function was evaluated by the peak filling velocity of E wave and A wave, E/A ratio, and deceleration time of E wave. The pulmonary systolic arterial pressure was also estimated in patients with tricuspid insufficiency. RESULTS: Right and left atrium and right ventricle diameters were significantly enlarged in cirrhotic patients versus controls. E/A ratio was decreased (p < 0.05) in patients with ascites (0.9 +/- 0.2) versus those without ascites (1.3 +/- 0.4) and controls (1.3 +/- 1). The estimated pulmonary systolic arterial pressure was slightly elevated in patients with ascites (35 +/- 5 mm Hg, six patients) versus those with no ascites (28 +/- 5, 10 patients) and controls (27 +/- 8, 6 controls, analysis of variance, p < 0.05). The pattern of left ventricular geometry was normal in the majority of patients. Nitrite and nitrate levels were increased in cirrhotics irrespective of the presence of ascites. CONCLUSIONS: Liver cirrhosis is associated with enlarged right cardiac chambers. Diastolic dysfunction and mild pulmonary hypertension are evident in cirrhotic patients with ascites. These changes do not depend on variations in the left ventricular geometry.     

Cardiac consequences of renal transplantation: changes in left ventricular morphology and function

To characterize changes in left ventricular morphology and function associated with renal transplantation, noninvasive cardiac evaluations were performed in 41 adults at the time of surgery and at follow-up. At the time of transplantation, 36 patients had undergone hemodialysis through a fistula for 2.3 +/- 2.5 years (mean +/- SD); their hematocrit level was 26 +/- 6% and systolic blood pressure was 151 +/- 19 mm Hg. Perioperatively, left ventricular hypertrophy was present in 93% of patients by echocardiography, but in only 37% by electrocardiography. Abnormal left ventricular diastolic function was present in 67% of patients and indicated a high risk for perioperative pulmonary edema. At follow-up (1.5 +/- 1.4 years), mean hematocrit level increased to 39 +/- 7%, systolic blood pressure decreased to 132 +/- 14 mm Hg and spontaneous closure of the fistula occurred in 13 patients. Left ventricular mass by echocardiography decreased from 237 +/- 66 to 182 +/- 47 g (p less than 0.001), a decrease of 23%. Left ventricular volumes and cardiac index also decreased significantly, reflecting the rapid resolution of a pretransplant high output state. Despite proportionate regression of left ventricular hypertrophy within months of transplantation, diastolic function did not improve. The significant regression of left ventricular hypertrophy that occurs after renal transplantation may help explain the improved cardiovascular survival of patients with a renal transplant over that of patients on long-term dialysis.     

Experimental congestive heart failure produced by rapid ventricular pacing in the dog: cardiac effects

Chronic rapid ventricular pacing in the dog reportedly produces a useful preparation of low-output heart failure. However, little information is available regarding cardiac changes in this preparation. Accordingly, we evaluated the effects of both short-term (3 weeks) and prolonged (2 months) rapid ventricular pacing on cardiac hemodynamics, mass, and chamber size. The effects of short-term pacing on left ventricular wall thickening, blood flow, and metabolism were also examined. Compared with 16 control dogs, dogs paced for either 3 weeks (n = 8) or 2 months (n = 13) exhibited reduced cardiac outputs (control 130 +/- 20 ml/min/kg, 3 week pacing 112 +/- 19 ml/min/kg, 2 month pacing 116 +/- 14 ml/min/kg) and elevated pulmonary wedge pressures (control 10 +/- 3 mm Hg, 3 week pacing 26 +/- 5 mm Hg, 2 month pacing 26 +/- 8 mm Hg) and right atrial pressures (control 4 +/- 1 mm Hg, 3 week pacing 13 +/- 3 mm Hg, 2 month pacing 9 +/- 3 mm Hg) (all p less than .01 vs control). At the postmortem examination, both groups of paced dogs also exhibited increased left ventricular volumes (control 13 +/- 6 ml, 3 week pacing 27 +/- 6 ml, 2 month pacing 26 +/- 8 ml), right ventricular volumes (control 13 +/- 5 ml, 3 week pacing 27 +/- 9, 2 month pacing 24 +/- 7 ml), and right ventricular mass (control 27 +/- 5 g, 3 week pacing 32 +/- 6 g, 2 month pacing 34 +/- 6 g) (all p less than .03 vs control) but had normal left ventricular mass. Three weeks of pacing also decreased percent left ventricular shortening (34 +/- 6% to 17 +/- 7%) associated with a disproportionate deterioration of posterior wall thickening (58 +/- 16% to 17 +/- 18%) (both p less than .01), as assessed by echocardiography. This left ventricular dysfunction was associated with no change in myocardial lactate extraction (prepacing 40 +/- 10%, 3 week pacing 36 +/- 10%), myocardial arteriovenous O2 difference, or myocardial histology, suggesting that it was not due to myocardial ischemia. These data indicate that rapid ventricular pacing in the dog produces a useful experimental preparation of low-output heart failure characterized by biventricular pump dysfunction, biventricular cardiac dilation, and nonischemic impairment of left ventricular contractility.     

Echocardiographic assessment of left ventricular hypertrophy and function in renal hypertensive dogs

To investigate the performance of the hypertrophied left ventricle, M-mode echocardiographic measurements were performed 2 to 3 times weekly on 8 unanesthetized dogs for several weeks before and for 6 months after the induction of perinephritic hypertension. Four dogs with sham-wrapping and contralateral nephrectomy served as the controls. From a baseline value of 7.7 +/- 0.4 mm (mean +/- SD), left ventricular wall thickness increased to 9.0 +/- 0.6 mm (p less than 0.001) by the 4th week after the induction of hypertension and reached a plateau of 10.2 +/- 1.2 mm (p less than 0.001) by week 10. Fractional shortening of left ventricular dimension (% delta D) increased during early left ventricular hypertrophy and remained elevated for 6 months in the surviving 6 hypertensive dogs. In hypertensive dogs, left ventricular concentric hypertrophy became detectable by week 6 of hypertension. Control dogs did not show these changes. At autopsy, the left ventricular weight of hypertensive and normotensive control dogs was (6.2 +/- 1.4 g/kg and 4.3 +/- 0.5 g/kg (p less than 0.05). In summary, during the early stage of left ventricular hypertrophy in renal hypertensive dogs cardiac performance increased. There is no evidence for deterioration of left ventricular performance as concentric left ventricular hypertrophy develops and becomes chronic.     

Haemodynamic adaptation two months after transjugular intrahepatic portosystemic shunt (TIPS) in cirrhotic patients.

BACKGROUND AND AIMS: In portal hypertensive patients, transjugular intrahepatic portosystemic shunt (TIPS) acutely increases cardiac output and exaggerates peripheral vasodilatation. It has been suggested that the worsened hyperdynamic state may progress to high output heart failure. The aim was to evaluate the acute and short-term haemodynamic adaptation to this procedure. METHODS: Systemic, splanchnic, and pulmonary haemodynamics were studied in 15 cirrhotic patients under stable haemodynamic conditions before placement of TIPS, then 15-30 minutes after and two months later. For inclusion in the final analysis, an uneventful post-TIPS at two months follow up and a stable portacaval gradient were required. The following variables were measured or calculated: portacaval gradient; cardiac index (thermodilution); systolic and diastolic mean arterial, atrial, pulmonary arterial, and wedged pulmonary capillary pressures; heart rate; and total peripheral and pulmonary vascular resistances. Blood flow in the shunt was measured using duplex Doppler ultrasound. RESULTS: The portacaval gradient decreased by 56% and remained stable thereafter. Shunt blood flow was unchanged when measured immediately after TIPS and two months later. Immediately after TIPS there was a pronounced increase in cardiac index (+32%; p < 0.05) in association with a decrease in peripheral and pulmonary vascular resistance (-21%; p < 0.05 and -14%; NS). Two months later, whereas the initial rise in cardiac index was attenuated, peripheral vascular resistances remained similar and pulmonary vascular resistances decreased further (-33%; p < 0.05) compared with immediate post-TIPS values. CONCLUSIONS: Hyperdynamic circulation worsened immediately after TIPS, with a progressive adaptation during follow up. The mechanisms of post-TIPS induced haemodynamic changes include an abrupt volume load resulting from splanchnic decompression and an increased delivery of gut derived vasodilators to the systemic circulation. The persistence of decreased peripheral and pulmonary vascular resistances despite the reduction in high cardiac output two months after TIPS suggests that vasodilatation is not solely a compensatory response to a TIPS induced increased preload. Vasodilatory substances shunted away from the liver probably play an important part in this phenomenon.     

Cardiac function and haemodynamics in alcoholic cirrhosis and effects of the transjugular intrahepatic portosystemic stent shunt

BACKGROUND: A portosystemic stent shunt may impair cardiac function and haemodynamics. AIMS: To investigate the effects of a transjugular intrahepatic portosystemic shunt (TIPS) on cardiac function and pulmonary and systemic circulation in patients with alcoholic cirrhosis. PATIENTS/METHODS: 17 patients with alcoholic cirrhosis and recent variceal bleeding were evaluated by echocardiography and catheterisation of the splanchnic and pulmonary circulation before and after TIPS. The period of catheter measurement was extended to nine hours in nine of the patients. The portal vein was investigated by Doppler ultrasound before and nine hours after TIPS. RESULTS: Baseline echocardiography showed the left atrial diameter to be slightly increased and the left ventricular volume to be in the upper normal range. Nine hours after TIPS, the left atrial diameter and left ventricular end diastolic volume were increased (by 6% (p<0.01) and 7% (p<0.01) respectively); end systolic volume had not changed significantly. Invasive measurements showed a sharp increase in right atrial pressure (by 101%; p<0.01), mean pulmonary artery pressure (by 92%; p<0.01), pulmonary capillary wedge pressure (by 111%; p<0.01), and cardiac output (8.1 (1.6) to 11.9 (2.4) l/min; p<0.01). Systemic vascular resistance decreased (824 (242) to 600 (265) dyn.s.cm-5 p<0.01), and total pulmonary resistance increased (140 (58.5) to 188 (69.5) dyn.s.cm-5; p<0.05). Total pulmonary resistance (12%; NS), cardiac output (1.4 l/min; p<0. 05), and portal vein blood flow (1.4 l/min; p<0.05) remained elevated for nine hours after TIPS in the subgroup. Portoatrial pressure gradient (43%; p<0.05), portohepatic vascular resistance (72%; p<0.05), and systemic vascular resistance (27%; p<0.01) were consistently reduced. CONCLUSIONS: The increase in the left atrial diameter, the pulmonary capillary wedge pressure, and total pulmonary resistance observed after the TIPS procedure reflected diastolic dysfunction of the hyperdynamic left ventricle in patients with alcoholic cirrhosis. The haemodynamic effects of the portosystemic stent shunt itself on the splanchnic circulation seem to be mainly responsible for the further decrease in systemic vascular resistance. TIPS may unmask a coexisting preclinical cardiomyopathy in patients with alcoholic cirrhosis and portal hypertension.     

Pathophysiology of impaired right and left ventricular function in chronic embolic pulmonary hypertension: changes after pulmonary thromboendarterectomy

STUDY OBJECTIVES: This study sought to evaluate the pathophysiology of left and right heart failure in patients with chronic thromboembolic pulmonary hypertension (CTEPH) who were hospitalized to undergo pulmonary thromboendarterectomy (PTE). DESIGN: Thirty-nine patients (16 women and 23 men; mean +/- SD age, 55+/-12 years) with severe CTEPH were examined before and 13+/-8 days after PTE by way of transthoracic echocardiography and right heart catheterization. MEASUREMENTS AND RESULTS: Examination results confirmed in all cases that before surgery the right ventricles were enlarged and systolic function was impaired. Moderate to severe tricuspid valve regurgitation was observed. Left ventricular eccentricity indexes reflected a leftward displacement of the interventricular septum. End-diastolic left ventricular size and systolic function had decreased, and the left ventricular filling pattern showed impaired diastolic function. After surgery, mean pulmonary artery pressure was significantly lower (48+/- 10 mm Hg vs. 25+/-7 mm Hg; p<0.05). The calculated end-diastolic and end-systolic right ventricular areas had decreased: 30+/-7 cm(2) vs 21 +/-5 cm(2) (p<0.05) and 24+/-6 cm(2) vs. 14+/-4 cm(2) (p<0.05), respectively. Right ventricular fractional area change had increased (20+/-7% vs. 33+/-8%; p<0.05). Most of the patients exhibited a marked decrease in the severity of tricuspid regurgitation. Septal motion, left ventricular systolic function, and diastolic filling pattern returned to normal values (early to late diastolic left ventricular inflow ratio, 0.70+/-0.33 vs. 1.35+/-0.51; p<0.05). The mean cardiac index also improved (2.7+/-0.6 L/min/m(2) vs. 3.7+/-0.8 L/min/m(2)). CONCLUSIONS: In CTEPH, functions are impaired in the right as well as the left ventricles of the heart. Improved lung perfusion and the reduction of right ventricular pressure overload are direct results of PTE, which in turn bring a profound reduction of right ventricular size and a recovery of systolic function. Normalization of interventricular septal motion as well as improved venous return to the left atrium lead to a normalization of left ventricular diastolic and systolic function, and the cardiac index improves.     

The importance of pericardial constraint in experimental pulmonary embolism and volume loading.

To clarify the magnitude of the contribution of pericardial constraint to the hemodynamic deterioration that is observed during acute pulmonary embolism, hemodynamics and chamber dimensions (sonomicrometry) were measured during pulmonary embolization and subsequent volume loading in six anesthetized and instrumented open-chest, open-pericardium dogs. Embolization markedly increased peak right ventricular systolic pressure (38 +/- 5 mm Hg before embolism to 64 +/- 12 mm Hg after repeated embolization, p less than 0.05). However, right ventricular stroke volume decreased by only an insignificant amount (17 +/- 7 ml to 15 +/- 6 ml, p = not significant). Indices of left ventricular end-diastolic volume (left ventricular area = anteroposterior x septum-to-left ventricle free wall diameters) and stroke work (stroke work = area of the left ventricular pressure-area loop) were also similar before and after repeated embolization. Volume loading after repeated embolization resulted in increased right ventricular stroke volume (15 +/- 6 ml to 20 +/- 4 ml, p = 0.06), left ventricular area (3320 +/- 600 mm2 to 3470 +/- 580 mm2, p less than 0.05) and stroke work (261 +/- 158 mm Hg to 425 +/- 170 mm Hg x mm2, p less than 0.05). These results are in marked contrast to those in a previously reported study in a closed-chest and closed-pericardium model in which there was a decrease in left ventricular preload and systolic function after similar embolization-induced right ventricular pressure loading. Moreover, there was a further decrease in these parameters as a result of volume loading after embolism in the closed pericardium experiments. In conclusion, pericardial constraint contributes to hemodynamic deterioration during both acute right ventricular pressure loading and subsequent volume loading. The hemodynamic response to both interventions in the intact animal is determined not only by the degree of right ventricular dysfunction but also by the degree of direct ventricular interaction.     

Early cardiac changes related to radiation therapy

To investigate the incidence and severity of possible radiation-induced cardiac changes, 21 women without heart disease were investigated serially by echocardiography and by measuring systolic time intervals before and up to 6 months after postoperative radiation therapy because of breast cancer. Radiation was associated with a decrease in fractional systolic shortening of the left ventricular (LV) minor-axis diameter, from 0.35 +/- 0.05 to 0.32 +/- 0.06 (p less than 0.005), and in the systolic blood pressure/end-systolic diameter ratio, from 4.4 +/- 1.2 to 3.9 +/- 0.9 mm Hg/mm (p less than 0.005). The mitral E point-septal separation increased, from 2.8 +/- 1.5 to 4.2 +/- 2.5 mm (p less than 0.005). The preejection period/LV ejection time ratio of systolic time intervals increased, but only the decrease within 6 months after therapy was significant (p less than 0.005). All these changes reflect slight transient depression of LV function, which became normalized within 6 months after therapy. Up to 6 months after therapy, a slight pericardial effusion was found in 33% of the patients. Hence, conventional radiation therapy appeared to cause an acute transient and usually symptomless decrease in LV function, and later, slight pericardial effusion in one-third of the patients.     

Effect of cardiac resynchronization therapy on left atrial appendage function and pulmonary venous flow pattern

BACKGROUND: Previous studies have shown improvement in left ventricular function and development of the reverse remodeling in the left ventricle and left atrium after cardiac resynchronization therapy (CRT). The aim of this study was to investigate the effect of CRT on left atrial appendage (LAA) function and pulmonary venous flow pattern. METHODS: Eighteen patients with systolic heart failure and complete left bundle branch block underwent implantation of biventricular pacemaker devices. In order to follow changes in LAA, transthoracic and transesophageal echocardiographic examinations were performed 1 week before and repeated 1 and 6 months after pacemaker implantation. RESULTS: CRT resulted in significant clinical improvement and decrease in NYHA functional class in 17 patients (94%). Maximum and minimum areas of left atrial appendage (LAAAmax and LAAAmin) decreased, with a concomitant increase in LAA ejection fraction. [LAAAmax: from 4.6+/-2 to 4.2+/-1.8 cm2 at the first (P < 0.001) and to 4.0+/-1.8 cm2 at the sixth month (P < 0.001); LAAAmin: from 2.7+/-1.3 to 2.3+/-1.2 cm2 at the first (P < 0.001) and to 2.2+/-1.2 cm2 at the sixth month (P < 0.001) and LAA ejection fraction: from 41+/-12% to 46+/-10% at the first (P = 0.007) and to 47+/-8% at the sixth month (P = 0.003)]. LAA active emptying and filling flow and pulmonary venous systolic velocities also increased after CRT. The appendage active emptying velocity correlated significantly with left ventricular ejection fraction (r = 0.50, P = 0.002), LAA ejection fraction (r = 0.51, P = 0.002), left atrial maximal volume, LAVmax (r = -0.44, P = 0.007), left atrial minimal volume, LAVmin (r = -0.50, P = 0.002) and pulmonary vein systolic flow velocity (r = 0.33, P = 0.05). CONCLUSION: Treatment of heart failure by CRT results with marked improvements in LAA function and increases pulmonary venous systolic velocity.     

A reversible pulmonary artery band: preliminary experience

Pulmonary artery banding has become an infrequently used surgical technique. However, if a band was developed that could be relieved without the need for open heart surgery, it is likely that pulmonary artery banding would be used more frequently in the management of infants with congenital heart disease. Such a pulmonary artery band was placed in seven 1 week old mongrel puppies by using a loop of an absorbable suture material (Vicryl). One dog died at 2 months as a result of right ventricular failure. The remaining six dogs underwent cardiac catheterization and pulmonary balloon angioplasty at 6 months of age. After measuring pulmonary artery, right ventricular and aortic pressures and performing a right ventricular angiogram, balloon angioplasty of the band site was performed. A 20 mm balloon angioplasty catheter (Medi-Tech) was used in all dogs. Balloon angioplasty decreased right ventricular pressure from 101 +/- 19 to 42 +/- 3 mm Hg (p less than 0.05) and right ventricular systolic outflow tract gradient from 59 +/- 14 to 7 +/- 2 mm Hg (p less than 0.03), and increased the size of the band site from 8.7 +/- 0.03 to 14.9 +/- 0.5 mm (p less than 0.01). All dogs were recatheterized 2 months after angioplasty and were then killed for pathologic evaluation. At follow-up catheterization, right ventricular pressure, right ventricular outflow tract gradient and pulmonary artery size at the band site remained at the values obtained immediately after angioplasty. Postmortem examination demonstrated that there was no evidence of pulmonary artery damage. Although these studies are preliminary, they suggest that a reversible pulmonary artery band can be performed.     

Experimental cardiac tamponade: a hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics to the phase of respiration

A hallmark of cardiac tamponade is pulsus paradoxus. However, the exact mechanism of pulsus paradoxus and the relation of left and right ventricular ejection dynamics remain controversial, with some studies suggesting an inverse relation in ventricular filling and ejection and others citing a more important role for the effects of right heart ejection dynamics delayed by transit through the pulmonary artery bed. To specifically reexamine this issue, six sedated but spontaneously breathing dogs were studied during experimental cardiac tamponade with use of extensive hemodynamic instrumentation and Doppler methods. During cardiac tamponade, left ventricular systolic pressure decreased from 125.8 +/- 12.1 to 81.7 +/- 26.7 mm Hg (p less than 0.01) and cardiac output from 5.86 +/- 1.48 to 2.34 +/- 0.98 liters/min (p less than 0.001); mean pericardial pressure increased from -1.2 +/- 0.8 to 10.5 +/- 3 mm Hg (p less than 0.001) and pulsus paradoxus from 4.3 +/- 1.6 to 10.7 +/- 1.2 mm Hg (p less than 0.001) compared with baseline values. An inverse relation in left and right ventricular ejection dynamics that was very close to 180 degrees out of phase was seen throughout the respiratory cycle in multiple hemodynamic and Doppler variables including peak systolic pressures, aortic and pulmonary flow velocities and ventricular ejection times. Simultaneous recording of the transmitral pressure gradient provided indirect evidence that the ventricular ejection dynamics were directly related to changes in ventricular filling. However, the magnitude of ventricular pressure or output flow velocity for each respiratory cycle was variable, depending on the exact timing of filling and ejection in relation to the phase of respiration. Variation in left ventricular output due to changes in right ventricular output delayed by transit through the pulmonary vasculature was not recognized in any animal. It is concluded that in spontaneously breathing dogs with acute cardiac tamponade, peak ventricular pressures, ventricular ejection times and pulmonary and aortic flow velocities have an inverse relation that is very close to 180 degrees out of phase.     

Left ventricular remodeling after pulmonary autograft replacement of the aortic valve (Ross operation)

BACKGROUND AND AIM OF THE STUDY: Aortic valve replacement (AVR) with a pulmonary autograft is an alternative treatment for young patients with aortic valve disease. Superior hemodynamic performance of the pulmonary autograft, and impact on parameters of left ventricular function were analyzed. METHODS: Thirty patients (21 males, nine females; mean age 29.97+/-12.29 years; range: 6-54 years) underwent a Ross procedure between November 1997 and November 1999. Seven patients (23%) were children (aged <15 years). In total, 22 patients were analyzed; each had at least three months follow up. Eleven patients had predominant aortic stenosis (AS), and 11 had aortic insufficiency (AI). RESULTS: There were no operative deaths. Two patients developed severe insufficiency, and the autograft was replaced with a mechanical valve. Pre- and postoperative echocardiograms were reviewed. The mean neoaortic maximal gradient was 7.85+/-5.59 mmHg (range: 3-29 mmHg). AS patients showed reduced interventricular septal (IVS) thickness at one month (from 13.27+/-3.69 to 11.60+/-2.44 mm; p = 0.0165) and 18 months after surgery (p = 0.0104). Left ventricular posterior wall (LVPW) thickness was reduced from 12.04+/-3.75 to 9.48+/-2.47 mm (p = 0.0338) at one month and 18 months (p= 0.0128) after surgery. The left ventricular end-diastolic internal dimension (LVIDd) decreased from 50.71+/-10.20 to 44.98+/-7.29 mm (p = 0.0491) at one month after surgery. In AI patients, LVPW and IVS thicknesses showed no significant variation, and LVIDd was decreased at one month (from 68.50+/-8.39 to 59.04+/-9.21 mm; p = 0.0017) and 18 months (p = 0.0229) after surgery. Left ventricular end-systolic internal dimension (LVIDs) decreased from 44.06+/-6.39 to 39.03+/-7.99 mm (p = 0.0081) at three months after surgery. Left ventricular mass index (LVMI) in the AS group decreased from 179.01+/-62.26 to 115.74+/-37.62 g/m2 (p = 0.0021) at one month after surgery, and at 18 months was normal, with a decrease from 208.77+/-32.89 to 95.89+/-28.82 g/m2 (p= 0.0003) (n = 5). In the AI group, LVMI decreased from 186.25+/-85.21 to 140.58+/-62.02 g/m2 (p = 0.0011) at one month after surgery, and at 18 months from 217.70+/-98.02 to 146.73+/-84.55 g/m2 (p= 0.0131) (n = 5). CONCLUSION: The pulmonary autograft procedure can be used safely to replace the aortic valve, and allows optimal hemodynamic performance, with no significant aortic regurgitation. The Ross procedure results in normalization of left ventricular dimensions and improvement of left ventricular function early in the postoperative period.     

Reduction in left ventricular volume and improvement in hemodynamics following intravenous administration of pimobendan (UDGG 115 BS) in dilated cardiomyopathy

Acute cardiovascular effects of 5 mg (group I, n = 6) and 10 mg (group II, n = 6) i.v. pimobendan (UDCG 115 BS) were studied by right and left heart catheterizations in patients suffering from idiopathic dilated cardiomyopathy (NYHA II and III). Before and 2.5 h after application of pimobendan left ventricular volumes and left ventricular dP/dtmax were evaluated by left heart catheterization. Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCP), cardiac output (CO), heart rate, and systemic blood pressure were assessed before and 2.5, 4, and 6 h after administration of pimobendan. PCP was reduced from 12.2 +/- 7.5 to 8.3 +/- 7.1 mm Hg (p less than 0.05) by 5 mg of pimobendan, and from 18.3 +/- 6.2 to 6.2 +/- 3.4 mm Hg (p less than 0.005) by 10 mg of pimobendan. Reduction of RAP was significant only in group II (from 6.2 +/- 3.2 to 1.2 +/- 0.9 mm Hg; p less than 0.05). In contrast to other hemodynamic parameters, the significant increase of CO exhibited no dose-dependency. Only 10 mg of pimobendan induced a temporary reduction of mean arterial blood pressure. An increase in heart rate occurred only in group I and was merely transient. Left ventricular end diastolic and end systolic volume indices were clearly reduced by 5 mg as well as by 10 mg of pimobendan. A significant rise of left ventricular ejection fraction occurred only in group II. However, left ventricular dP/dtmax was increased significantly in both groups. No adverse effects were noted during acute administration of pimobendan. Therefore, intravenous pimobendan may be a useful drug in the treatment of acute cardiac failure.     

Early improvement in left ventricular diastolic function after relief of chronic right ventricular pressure overload

Chronic right ventricular pressure overload is associated with left ventricular diastolic dysfunction. Whether or not an abrupt reduction in pulmonary artery pressure in patients with chronic pulmonary hypertension results in early improvement of left ventricular diastolic function is unknown. To assess this, the Doppler indexes of left ventricular diastolic function and echocardiographic measures of left ventricular volume were analyzed in 22 patients (age, 41 +/- 14 years, mean +/- SD) before and within 1 week after pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension. Mean duration of cardiopulmonary symptoms was 37 months (range, 4 months to 9 years). After operation, mean pulmonary artery pressure and pulmonary vascular resistance decreased (50 +/- 13 to 29 +/- 9 mm Hg and 904 +/- 654 to 283 +/- 243 dynes.sec/cm5, respectively, both p less than 0.001), pulmonary artery wedge pressure was unchanged (11 +/- 5 to 12 +/- 5 mm Hg), and cardiac index increased (2.0 +/- 0.5 to 2.8 +/- 0.7 l/min/m2 p less than 0.001). Left ventricular end-diastolic volume and stroke volume increased significantly (58.5 +/- 18.0 to 76.6 +/- 25.0 ml and 30.3 +/- 12.3 to 41.8 +/- 12.5 ml, respectively, both p less than 0.001) after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right ventricular function assessed by two-dimensional strain and tissue Doppler echocardiography in patients with pulmonary arterial hypertension and effect of vasodilator therapy

Two-dimensional strain echocardiography is a new method for the assessment of regional contractility. Thirty-seven patients with pulmonary arterial hypertension (mean age 56.4 +/- 11 years) and 38 normal subjects (mean age 58.3 +/- 12 years) underwent 2-dimensional echocardiography and tissue Doppler echocardiographic evaluation of right ventricular (RV) global function and regional contractility. Patients with pulmonary arterial hypertension additionally underwent 6-minute walking distance tests and right-sided cardiac catheterization before and after (8 +/- 3 months) vasodilator therapy. Moderate or severe RV dysfunction was present in all patients (2-dimensional strain of the basal segment of the RV free wall: -8.8 +/- 4.1% systolic longitudinal deformation) compared with normal subjects (-24.3 +/- 4.7% systolic longitudinal deformation, p < 0.001) and was improved with vasodilator therapy after 6 to 11 months (-13.3 +/- 6.2% systolic longitudinal deformation, p < 0.001).     

Left ventricular diastolic function during positive end-expiratory pressure. Impact of right ventricular ischemia and ventricular interaction.

The individual and additive effects of positive end-expiratory pressure (PEEP) and right coronary artery (RCA) occlusion on left ventricular end-diastolic pressure-volume relations (LVEDPVR) were examined in six anesthetized dogs. Right ventricular (RV) and left ventricular (LV) ejection fractions (EF), end-diastolic volume (EDV) and end-systolic volumes (ESV) were measured by thermodilution as PEEP was added before and after RCA occlusion. PEEP alone caused a decline in cardiac output, transmural left atrial pressure (LAP) (6.0 +/- 0.6 to 3.2 +/- 1.4 mm Hg, p less than 0.05), and LVEDV (49 +/- 3 to 36 +/- 4 ml, p less than 0.05). RVEDV, the mean slope (+/- SD) of the LVEDPVR (0.37 +/- 0.16 to 0.30 +/- 0.19) and LAP at a common LV volume (35 ml, V35) did not change with PEEP. RCA occlusion caused cardiac output and RVEF (38 +/- 5 to 27 +/- 5%, p less than 0.05) to decline and RVESV (25 +/- 4 to 33 +/- 6 ml, p less than 0.05) to increase. RVEDV, the slope of the LVEDPVR, and LAP at V35 were unchanged from baseline. The addition of PEEP after RCA occlusion caused cardiac output to decline further. However, unlike before occlusion, there was no change in LAP (6.5 +/- 1.3 to 5.0 +/- 1.4 mm Hg) despite a decline in LVEDV (47 +/- 3 to 29 +/- 6 ml, p less than 0.05). RVESV and RVEDV increased with PEEP after RCA occlusion as did LAP at V35. The slope of the mean LVEDPVR tended to increase (0.98 +/- 1.03).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mid-term echographic evaluation of systolic function after cardiac transplantation

The aim of this study was to analyse variations in left ventricular mass (LVM) and systolic function after cardiac transplantation and to evaluate eventual changes induced by the onset of systemic hypertension (HT). In a retrospective study, we selected the echocardiographic examinations of 42 patients performed at the end of the first month (M1), sixth month (M6), and at the end of follow-up (ME) after cardiac transplantation. The patients were divided into two groups (NT: n = 14; HT: n = 28) depending on whether hypertension occurred during follow-up. The average duration of follow-up was 12.8 +/- 6 months; this was comparable in the two groups. Mild left ventricular hypertrophy was observed from the first postoperative examination: M1 = 193 +/- 50 g; M6 = 199 +/- 62 g; ME = 197 +/- 45 g (NS). The hypertrophy was constant with time and related to wall thickening; it was associated with an increased left ventricular fractional shortening (FS) which decreased with time especially in the NT group (average/42 patients: M1 = 0.38 +/- 0.09; M6 = 0.34 +/- 0.08; ME = 0.35 +/- 0.05; p = 0.03 between M1 and ME). The influence of hypertension on the development of LVH and wall thickening was negligible. The role of transplant rejection should be considered: the repetition of episodes of rejection was less marked than the histological severity of rejection. The role of other factors (ischaemia, persistent haemodynamic abnormalities) is a matter of discussion.     

Doppler characterization of left ventricular diastolic function in cardiac amyloidosis

Sixty-four patients with primary systemic amyloidosis-53 with two-dimensional echocardiographic features of cardiac involvement (Group I) and 11 without cardiac involvement (Group II)--underwent Doppler echocardiographic assessment of left ventricular diastolic function. Pulsed wave Doppler recordings of left ventricular inflow velocities and pulmonary vein flow velocities with respiratory monitoring in these patients were compared with findings in a normal group. Patients in Group I showed striking abnormalities of left ventricular diastolic filling when classified into subgroups by mean left ventricular wall thickness: early greater than 12 but less than 15 mm; advanced greater than or equal to 15 mm. In early amyloidosis, relaxation was abnormal, with decreased peak early velocity (75 +/- 20 versus 86 +/- 16 cm/s; p less than 0.01), increased late velocity (71 +/- 22 versus 56 +/- 13 cm/s; p less than 0.01), decreased early to late velocity ratio (1.2 +/- 0.6 versus 1.6 +/- 0.5; p less than 0.01) and prolonged isovolumic relaxation time (87 +/- 15 versus 73 +/- 13 ms; p less than 0.01) compared with normal values. In advanced amyloidosis, there was a restrictive filling pattern with a markedly shortened deceleration time (148 +/- 50 versus 199 +/- 32 ms; p less than 0.001), decreased pulmonary vein peak systolic flow velocity (34 +/- 16 versus 54 +/- 12 cm/s; p less than 0.01) and increased diastolic flow velocity (55 +/- 20 versus 44 +/- 12 cm/s; p less than 0.01) compared with normal values. Group and the subgroup with early amyloidosis had similar flow velocity patterns. Thus, this study documents that in cardiac amyloidosis, a spectrum of diastolic filling abnormalities exists; the restrictive filling pattern is seen only in the advanced stages.     

Echocardiographic study of cardiac morphological and functional changes before and after parturition in pregnancy-induced hypertension

PURPOSE: To investigate the cardiac morphological and functional changes by echocardiography, before and after parturition in patients with pregnancy-induced hypertension (PIH). METHODS: The parameters related to cardiac morphology and left ventricular diastolic and systolic functions were compared before and after parturition in 32 patients with PIH and 24 normal pregnant (NP) women. RESULTS: Compared with NP women, the PIH patients had greater diameters of left atrium and left ventricle in end-diastole (LAd: 38.9 +/- 4.5 vs 34.6 +/- 4.4 mm, P = 0.0015; LVEDd: 51.2 +/- 5.8 vs 47.1 +/- 4.2 mm, P = 0.036) and lower E/A (1.2 +/- 0.2 vs 1.4 +/- 0.2, P = 0.009) and greater fractional shortening (FS) (39.8 +/- 6.5% vs 37.1 +/- 6.9%, P = 0.042) and ejection fraction (EF) (0.72 +/- 0.07 vs 0.66 +/- 0.08, P = 0.040). Pericardial effusion (PE) occurred in 31.3% and 16.7% of PIH and NP, respectively. The LAd and LVEDd in 70% and 47% patients with PIH resolved and PE disappeared in 80% of PIH patients postpartum. E/A ratio in PIH significantly increased after parturition, while the two patients with cardiac systolic dysfunction did not improve very much. CONCLUSIONS: Compared with normal pregnancy, the most significant cardiac morphological changes in PIH are the greater diameters of left atrium and left ventricle, thicker inter-ventricular septum (IVS), more PE, impaired left ventricular diastolic function, and increased systolic function. The PE could disappear in PIH and about half of other abnormalities could recover to be the level of normal pregnancy postpartum within 2 months.