Rationale: Exercise tolerance is decreased in patients with pulmonary hypertension (PH). It is unknown whether exercise intolerance in PH coincides with an impaired rest-to-exercise response in right ventricular (RV) contractility.Objectives: To investigate in patients with PH the RV exertional contractile reserve, defined as the rest-to-exercise response in end-systolic elastance (ΔEes), and the effects of exercise on the matching of Ees and RV afterload (Ea) (i.e., RV–arterial coupling; Ees/Ea). In addition, we compared ΔEes with a recently proposed surrogate, the rest-to-exercise change in pulmonary artery pressure (ΔPAP).Methods: We prospectively included 17 patients with precapillary PH and 7 control subjects without PH who performed a submaximal invasive cardiopulmonary exercise test between January 2013 and July 2014. Ees and Ees/Ea were assessed using single-beat pressure–volume loop analysis.Measurements and Main Results: Exercise data in 16 patients with PH and 5 control subjects were of suffici...

The effects of exercise on right ventricular contractility and right ventricular-arterial coupling in pulmonary hypertension.

SUMMARY
To determine whether during acute myocardial infarction (MI), ischemia and asynergy can develop in areas remote from the infarct zone, we undertook a two-part study. In part 1, 51 patients with recent infarction (15.6 ± 4.1 days after MI) and one-vessel disease of ≥ 70% stenosis by angiography underwent two-dimensional echocardiography (2-D echo). Using an 11-segment ventricular model, the 2-D echocardiograms were read blind and then compared with angiography to establish the distribution of regional asynergy for MI involving each of the three major coronary arteries. In part 2, 30 patients underwent 2-D echo 10.8 ± 3.1 hours after onset of symptoms of acute MI. All 30 patients underwent coronary angiography before discharge and 19 had repeat 2-D echo 4–13 days after MI. One-vessel asynergy was defined as abnormal motion confined to a single vascular region; remote asynergy was designated when abnormal motion was present in two or more vascular regions.
Of 30 patients with acute MI, eight had one-vessel disease (1VD) and 22 had multivessel disease (MVD) by angiography. Remote asynergy by 2-D echo was found in 17 patients with MVD (77%), but in none with 1VD (p < 0.01). Of the five MVD patients without remote asynergy, four had only a 70% stenosis of a second coronary vessel. Compensatory hyperkinesis was seen in four of the 1VD patients (50%), but in only one of the MVD patients (4.5%) (p = 0.005). Follow-up 2-D echo in 19 patients revealed improvement in the extent of asynergy in two of five 1VD patients (33%) and in 10 of 13 MVD patients (77%) (p = 0.06).
Thus, MI in the distribution of a single coronary vessel produces a distinctive, recognizable pattern of asynergy. The stress of infarcton may induce compensatory hyperkinesis in 1VD patients, whereas in MVD patients this stress may exceed the perfusion capacity of the additionally stenosed vessels and result in remote asynergy. Finally, the extent of early asynergy during acute myocardial infarction overestimates the extent of asynergy present after recovery from the infarct.

Echocardiographic Detection of Infarct-localized Asynergy and Remote Asynergy During Acute Myocardial Infarction: Correlation with the Extent of Angiographic Coronary Disease

To examine the interaction between normal and nonischemic areas of the left ventricle during acute ischemia, we implanted midwall ultrasonic segment length gauges in the ischemic zone and in nonischemic areas of the canine left ventricle. During acute ischemia, end-diastolic pressure and segment length in the nonischemic areas increased. There was no change from control in the segment length at the time of aortic valve opening and closure. Thus, in nonischemic areas, total segment shortening, as measured by the percent change in segment length from the time of end-diastole to aortic valve closure, increased. This was due to an increase in isovolumic shortening (end-diastole to aortic valve opening) with no change in ejection shortening (aortic valve opening to closure). The progressive increase in isovolumic shortening in nonischemic areas over time was directly paralleled by the progressive development of the isovolumic lengthening or bulge in the ischemic zone. Nonischemic areas, whether adjacent, on the opposite wall, or distant to the ischemic zone, all behaved similarly. Adrenergic blockade did not qualitatively alter these findings. We conclude that acute ischemia induces a mechanical disadvantage which is greater than just the loss of contractile function by the ischemic segment. Despite the apparent hyperfunction of nonischemic areas, the increased total segment shortening is expended in stretching the ischemic zone during isovolumic systole. As a result, there is no significant "compensatory" increase in ejection shortening in nonischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Serial assessment of left ventricular performance following coronary artery bypass grafting. Early postoperative results with myocardial protection afforded by multidose hypothermic potassium crystalloid cardioplegia

Although impairment of left ventricular function in acute myocardial infarction is closely related to extent of necrosis, function in the noninfarct zone also contributes to global performance and thus may be of prognostic importance. We evaluated left ventricular regional wall motion by the centerline chord method in 332 patients treated with intravenous tissue-type plasminogen activator (t-PA) in the multicenter Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I trial. All patients had acute contrast ventriculograms of suitable quality for analysis, and 266 patients had paired acute and day 7 ventriculograms. Enhanced function of the noninfarct zone was present during acute catheterization (+0.3 SD/chord) and was associated with preservation of the acute ejection fraction (p = 0.0001). Multiple linear regression analysis revealed the most powerful clinical factor associated with enhanced function of the noninfarct zone was the absence of multivessel disease (p = 0.0001). Clinical factors that were related weakly to noninfarct zone function included female gender (p = 0.08) and higher flow in the infarct artery (p = 0.03). Neither the degree of infarct zone dysfunction nor infarct location was associated with hyperkinesis of the noninfarct zone. In hospital, mortality was closely related to function in the noninfarct zone (p = 0.006), ejection fraction (p = 0.025), and the number of diseased vessels (p = 0.009) but was not related to infarct zone function (p = 0.128).(ABSTRACT TRUNCATED AT 250 WORDS)

Prognostic implications and predictors of enhanced regional wall motion of the noninfarct zone after thrombolysis and angioplasty therapy of acute myocardial infarction. The TAMI Study Groups.

The relationship of segmental left ventricular (LV) wall motion abnormalities to LV function 2-6 days after acute transmural myocardial infarction (MI) was investigated in 45 patients by quantitative contrast ventriculography. Patients were divided into four classes according to the MIRU criteria. Segmental wall motion was assessed by determining the percentage of systolic shortening (deltaS) along nine hemiaxes and the extent of akinetic or dyskinetic abnormally contracting segments (% ACS) expressed as a percentage of end-diastolic perimeter. When compared with that in 17 normal control-subjects, the LV end-diastolic volume was increased only in patients in class III and class IV; the LV end-systolic volume increased progressively from normal through class IV. Ejection fraction had a negative linear correlation with %ACS (r = 0.97). The size of ACS was larger in anterior (34 +/- 14%) than in inferior MIs (23 +/- 7%), resulting in greater LV dysfunction. However, for a comparable size of ACS, infarct location alone did not influence LV function parameters. In the noninfarcted zone, deltaS was increased when the size of ACS was less than 25% and reduced when the size of ACS was greater than 25%. Thus, the size of ACS is a major determinant of LV dysfunction in acute MI. The compensatory mechanisms operate either through an augmented mechanical function of residual myocardium when the infarct is small, or through the Frank-Starling mechanism when the infarct is large.

Regional left ventricular function assessed by contrast angiography in acute myocardial infarction.

Dobutamine was infused at a rate of 8 mcg/kg/min in 17 patients with or without congestive heart failure Cardiac output increased from an average 292 to 445 1/min/m2(p less than 0001) with no change in mean aortic pressure (934 to 978 mmHg) and only a slight increase in heart rate (78 to 87 beats/min) Left ventricular end-diastolic pressure decreased from an average 19 to 137 mmHg (p less than 001) Peak left ventricular dp/dt was doubled (1147 to 2370 mmHg/sec, p less than 0001) and Vmax increased from 108 to 218 circ/sec (p less than 0001) In 10 patients given equi-inotropic doses (100 per cent increase in peak dp/dt) Isoproterenol produced a greater increase in cardiac output (71 percent) than Dobutamine /51 percent) Isoproterenol caused mean aortic pressure to fall significantly (8 percent) while no change was noted with Dobutamine Accordingly, peripheral vascular resistances were reduced to a greater extent with Isoproterenol than with Dobutamine (p less than 005) Mean pulmonary arterial pressure decreased significantly (25 +/- 59 to 22 +/- 57 mmHg, p less than 005) with Isoproterenol infusion and remained unchanged with Dobutamine infusion Dobutamine increased both stroke work (57 percent) and minute work (83 percent) With Isoproterenol however, only minute work was significantly increased (90 percent) Dobutamine therefore is a potent inotropic drug, with mild chronotropic and peripheral vascular effect and may be valuable in the management of severe heart failure not associated with hypotension

Comparative haemodynamic effects of dobutamine and isoproterenol in man

Left ventricular end-diastolic pressure (P) and volume (V) were measured in 12 patients with acute myocardial infarction. It was assumed that the diastolic P-V relationship was exponential and corresponded to the formula P=be KV. In 7 patients submitted to volume loading, several data points of this relationship were obtained and at zero volume, the mean intercept with the ordinates was 0.037+/-0.015 kPa (SEM) (0.28+/-0.12 mmHg). In the other 5 patients, the P-V curve was plotted through this intercept and the pressure and volume co-ordinates obtained by control. The K coefficient (passive elastic modulus) was greater, and the normalised left ventricular compliance index (dV/VdP) was smaller in the infarct group than in the control group. This suggests decreased left ventricular compliance during the acute phase of myocardial infarction. By comparing left ventricular function curves plotted using either end-diastolic pressure or end-diastolic volume as the stretch index it is possible to evaluate the relative participation of decreased compliance and depressed contractility in global left ventricular function.

Left ventricular compliance in acute myocardial infarction in man

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Regional left ventricular function assessed by contrast angiography in acute myocardial infarction.

Comparative haemodynamic effects of dobutamine and isoproterenol in man

Left ventricular compliance in acute myocardial infarction in man