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PubMed1989

Hemodynamic effects of intravenous pimobendan in patients with left ventricular dysfunction.

Sequential hemodynamic effects of intravenous pimobendan (UD-CG 115 BS), a novel compound with positive inotropic and vasodilating properties, were investigated during left heart catheterization in nine patients with left ventricular dysfunction (ejection fraction less than or equal to 40%) and moderate congestive heart failure (NYHA classes II and III). Studies were carried out before (C) and for 60 min after intravenous administration of 5 mg of pimobendan over 1 min. Pimobendan immediately and progressively reduced systemic resistance [16 and 28% at 10 and 60 min postdrug, respectively (p less than 0.05 vs. C)] and left ventricular end diastolic pressure [from 24 +/- 3 (C) to 12 +/- 3 mm Hg at 60 min, p less than 0.001)]. Cardiac output gradually increased by 24%, but stroke volume did not, due to an equally progressive 14% rise in heart rate, whereas stroke work increased by 21% (all p less than 0.05 vs. C). Both contractility and relaxation, measured at fixed heart rates, significantly improved by 30 and 20%, respectively, at 50 min postdrug. Thus, pimobendan has immediate and prolonged arterial vasodilating effects, together with positive inotropic and lusitropic properties, resulting in an early but sustained improvement of left ventricular pump function and filling pressures.

Aged↗
PubMed1994

Patient perception of a long-term clinical trial: experience using a close-out questionnaire in the Studies of Left Ventricular Dysfunction (SOLVD) Trial. SOLVD Close-out Working Group.

A close-out questionnaire was distributed to the participants in a long-term heart failure trial, Studies of Left Ventricular Dysfunction (SOLVD). The respondents' primary motivation for enrollment, positive and negative experiences, and reported changes in habitual behavior was analyzed. Seventy-four percent (N = 3522) of the eligible patients responded to the survey. The most commonly cited reason for enrollment was recommendation by the primary physician. A wish "to contribute to medical science" and "to help others" was also a frequent incentive. A majority of the respondents were satisfied with participation and would be willing to participate in a future clinical trial. Most negative experiences included transportation to and from the clinic and frequent staff changes. A significant number of the patients reported changes in their smoking habits, alcohol intake, and diet despite the absence of behavioral interventions in the study protocol. There were minor differences between attitudes and perceptions of the male and female participants. No differences were found between patients who had previously participated in a clinical trial and those who had not.

Attitude↗
PubMed2003

Randomized, double-blind, placebo-controlled long-term study of isosorbide-5-mononitrate therapy in patients with left ventricular dysfunction after acute myocardial infarction.

BACKGROUND: Nitrates are often administrated with a variety of other pharmacologic agents in the management of chronic heart failure (CHF). However, limited information is available concerning the long-term effects in patients with evidence of left ventricular (LV) dysfunction after acute myocardial infarction (AMI) already treated with standard heart failure therapy. METHODS: In a randomized, double-blind, placebo-controlled trial, we evaluated the effects of a 60 mg dose of isosorbide-5-mononitrate (IS-5-MN) given daily for 11 months to 47 patients with clinical or echocardiographic evidence of left ventricular dysfunction after acute myocardial infarction. Forty-five patients received a placebo. RESULTS: Invasive hemodynamic measurements did not show any difference between the treatment regimens. Overall changes in echocardiographic measurements were not significantly different between IS-5-MN therapy and the placebo groups. However, in a prespecified subgroup with left ventricular ejection fraction < or =40% at baseline, IS-5-MN therapy resulted in a lesser increase of end-diastolic volume index than the placebo (P =.047). IS-5-MN significantly reduced the serum concentration of atrial natriuretic peptide (mean 20.0 pmol/L, 95% CI 7.7-32.3, P =.002), whereas the placebo did not (P =.041 for the difference between the groups). The proportion of patients taking diuretics was significantly reduced in the IS-5-MN group, from 30 of 44 to 20 of 44 (P =.02), but not with placebo, which remained at 27 of 43 (P = 1.0, with P =.048 for the difference between the regimens). CONCLUSIONS: Oral, long-term IS-5-MN therapy resulted in lower atrial natriuretic peptide levels and reduced the need for additional diuretics. Less LV dilatation was observed in patients with more severe LV dysfunction at baseline.

Aged↗
PubMed1988

Hemodynamic comparison of dopexamine hydrochloride and dopamine in ischemic left ventricular dysfunction.

The hemodynamic dose-response effects of intravenous dopexamine hydrochloride (0.5 to 2.0 micrograms/kg/min) have been compared with dopamine (2.5 to 10 micrograms/kg/min) in 12 patients with ischemic left ventricular dysfunction in an open randomized crossover study. Both drugs increased cardiac output and decreased systemic vascular resistance. Dopexamine hydrochloride appeared to increase heart rate more than dopamine although this did not reach statistical significance. Dopexamine hydrochloride produced small increases in systolic and decreases in diastolic blood pressure, whereas dopamine had a biphasic effect resulting in a decrease in mean blood pressure at low doses and an increase at the highest dose studied. With increasing dosage, there was a trend toward more vasodilator activity with dopexamine hydrochloride than with dopamine. Dopexamine hydrochloride produced fewer adverse effects than dopamine.

Adult↗
PubMed1998

Time course of sympathovagal imbalance and left ventricular dysfunction in conscious dogs with heart failure.

To elucidate the time course of sympathovagal balance and its relationship to left ventricular function in heart failure, we serially evaluated left ventricular contractility and relaxation and autonomic tone in 11 conscious dogs with tachycardia-induced heart failure. We determined a dynamic map of sympathetic and parasympathetic modulation by power spectral analysis of heart rate variability. The left ventricular peak +dP/dt substantially fell from 3,364 +/- 338 to 1,959 +/- 318 mmHg/s (P < 0.05) on the third day and declined gradually to 1,783 +/- 312 mmHg/s at 2 wk of rapid ventricular pacing. In contrast, the time constant of left ventricular pressure decay and end-diastolic pressure increased gradually from 25 +/- 4 to 47 +/- 5 ms (P < 0.05) and from 10 +/- 2 to 21 +/- 3 mmHg (P < 0.05), respectively, at 2 wk of pacing. The high-frequency component (0.15-1.0 Hz), a marker of parasympathetic modulation, decreased from 1,928 +/- 1,914 to 62 +/- 68 x 10(3) ms2 (P < 0.05) on the third day and further to 9 +/- 12 x 10(3) ms2 (P < 0.05) at 2 wk. Similar to the time course of left ventricular diastolic dysfunction, plasma norepinephrine levels and the ratio of low (0.05- to 0.15-Hz)- to high-frequency component increased progressively from 135 +/- 50 to 532 +/- 186 pg/ml (P < 0.05) and from 0.06 +/- 0.06 to 1.12 +/- 1.01 (P < 0.05), respectively, at 2 wk of pacing. These cardiac and autonomic dysfunctions recovered gradually toward the normal values at 2 wk after cessation of pacing. Thus a parallel decline in left ventricular contractility with parasympathetic influence and a parallel progression in left ventricular diastolic dysfunction with sympathoexcitation suggest a close relationship between cardiac dysfunction and autonomic dysregulation during development of heart failure.

Animals↗
PubMed1995

Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease.

Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.

Antihypertensive Agents↗
PubMed2003

Utility of B-type natriuretic peptide (BNP) as a screen for left ventricular dysfunction in patients with diabetes.

OBJECTIVE: Routine screening of diabetic patients with echocardiography is not feasible due to its limited availability and high cost. B-type natriuretic peptide (BNP) is secreted from the left ventricle in response to pressure overload and is elevated in both systolic and diastolic dysfunction. RESEARCH DESIGN AND METHODS: BNP levels were compared to echocardiographic findings in 263 patients. Patients were divided into two groups: clinical indication for echocardiography (CIE) (n = 172) and those without clinical indication for echocardiography (no-CIE) (n = 91). Cardiologists making the assessment of left ventricular function were blinded when measuring plasma levels of BNP. RESULTS: The 91 patients with no-CIE with echoes had similar BNP levels (83 +/- 16 pg/ml) to the 215 patients with no-CIE without echoes (63 +/- 10, P = 0.10). Patients with CIE and subsequent abnormal left ventricular function (n = 112) had a mean BNP concentration of 435 +/- 41 pg/ml, compared with those with no-CIE, but had abnormal left ventricular function on echo (n = 32) (161 +/- 40 pg/ml). Twenty-one of 32 patients with no-CIE but with abnormal left ventricular function had diastolic dysfunction (BNP 190 +/- 60 pg/ml). A receiver-operating characteristic (ROC) curve revealed that the area under the curve was 0.91 for CIE patients and 0.81 for no-CIE patients (P < 0.001). For those with no congestive heart failure (CHF) symptoms, BNP levels showed a high negative predictive value (91% for BNP values <39 pg/ml), while in those patients who had a CIE, BNP levels showed a high positive predictive value for the detection of left ventricular dysfunction (96% with BNP levels >90 pg/ml). CONCLUSIONS: BNP can reliably screen diabetic patients for the presence or absence of left ventricular dysfunction.

Atrial Fibrillation↗
PubMed2001

Increased brain natriuretic peptide as a marker for right ventricular dysfunction in acute pulmonary embolism.

Right ventricular (RV) function is of major prognostic significance in patients with acute pulmonary embolism (PE). The aim of the present study was to evaluate the role of neurohormone plasma brain natriuretic peptide (BNP) in assessing RV function in patients with acute PE. BNP levels were measured in 16 consecutive patients with acute PE as diagnosed by high probability lung scintigraphy or pulmonary angiography. Twelve healthy age-matched volunteers served as controls. All 16 patients underwent standard echocardiography and blood tests during the first hour of presentation. In the patient group, survival was studied for a period of 30 days. Plasma BNP levels in patients with acute PE were higher than in controls (7.2 [95% CI 0.4 to 144.6] versus 1.4[95% CI 0.4 to 4.6] pmol/L, p = 0.0008). Plasma BNP was significantly higher in 5 patients with RV dysfunction compared to II patients with normal RV function (40.2 [95% CI 7.5 to 214.9] versus 3.3 [95% CI 0.4 to 24.9] pmol/L, p = 0.0003). RV systolic pressure was not significantly correlated with BNP (r = 0.42, p = ns). In conclusion, plasma BNP neurohormone levels might be of clinical importance as a supplementary tool for assessment of RV function in patients with acute PE.

Acute Disease↗
PubMed1984

Vasodilator therapy in children: acute and chronic effects in children with left ventricular dysfunction or mitral regurgitation.

To determine the acute and chronic effects of vasodilator therapy in children, vasodilator therapy was evaluated in 13 children (aged 0.2 to 14.5 years) with severe left ventricular dysfunction or mitral regurgitation. In seven children, nitroprusside increased cardiac index by an average of 33% (P less than .01) and increased stroke index by 29% (P less than .01). In eight children, hydralazine caused a 31% increase in cardiac index (P less than .01) and a 27% increase in stroke index (P less than .02). Ten children received chronic oral vasodilator therapy and were followed for 5.7 +/- 1.4 (SEM) months. Early clinical improvement was observed in every child. Symptoms of heart failure diminished in all, and five children became entirely asymptomatic. A significant (P less than .05) improvement was noted in growth velocity, respiratory rate, heart size, and incidence of gallop rhythm after 1 month of therapy. The duration of the beneficial response to vasodilator therapy varied considerably, however, and significant improvement for the group was not found after 1 month. Four children had sustained clinical improvement for 6 months or longer, but the others experienced recurrent heart failure within 1 to 4 months.

Adolescent↗
PubMed1992

Effect of diltiazem on norepinephrine-induced acute left ventricular dysfunction.

The present study has examined the role of diltiazem as a protective agent in a canine model of norepinephrine cardiotoxicity. Effects of diltiazem, 20 micrograms/kg/min x 5 min pretreatment followed by 10 micrograms/kg/min x 90 min, or saline infusion were examined at baseline and 1 h after infusion of norepinephrine, 4 micrograms/kg/min for 90 min, in closed-chest anesthetized dogs. Left ventricular function was assessed by equilibrium radionuclide angiogram and two-dimensional echocardiogram. In 7 saline experiments, hypotension and increased heart rate were observed at 1 h post infusion. In the diltiazem-treated group (n = 7), mean arterial pressure and heart rate were unchanged. In the saline group, left ventricular ejection fraction fell from 0.50 +/- 0.04 to 0.28 +/- 0.04. Left ventricular ejection fraction was unchanged in the diltiazem-treated group: 0.52 +/- 0.03 to 0.55 +/- 0.07. Left ventricular end-diastolic volume was increased at 1 h post infusion in saline controls but not in the diltiazem-treated group. Measurement of fractional shortening from two-dimensional echocardiograms also indicated left ventricular dysfunction in the saline but not diltiazem-treated groups. Left ventricular end-systolic wall stress following norepinephrine infusion was significantly increased in the saline but not diltiazem-treated groups: 122.7 +/- 18.7 vs 67.6 +/- 19.7 g/cm2, respectively. In dogs receiving saline without norepinephrine infusion, no significant changes occurred over the course of the experiment. Histologic examination showed mild contraction band necrosis in saline controls but not in sham saline dogs. Diltiazem showed intermediate histologic evidence of injury, which was not further quantified. This study suggests that effects of norepinephrine on left ventricular function in the canine model of norepinephrine cardiotoxicity may be largely due to increased wall stress following a prolonged increase in afterload. Diltiazem pretreatment afforded significant protection of left ventricular function.

Animals↗
PubMed1994

[Plasma levels of basal beta-endorphin and after effort in patients with severe left ventricular dysfunction and heart failure].

BACKGROUNDS: Purpose of the study was to evaluate beta-endorphin plasma levels at rest and after exercise, and the beta-endorphin release, in relation to exercise capacity, in patients with severe left ventricular dysfunction and heart failure. METHODS: Beta-endorphin plasma levels were assayed by radio-immunoassay before and after cardiopulmonary exercise testing in 28 heart failure patients with radionuclide ejection fraction < 35%, left ventricular end-dyastolic dimension > 60 mm and heart failure, and in 9 age-matched normal subjects. According to Weber's classification, 10 patients were in class A, 9 in class B, and 9 in class C. RESULTS: Beta-endorphin plasma levels at rest were respectively 3.52 +/- 2.31 pmol/L in patients, and 1.77 +/- 0.84 pmol/L (p < 0.05) in normals. In patients, baseline beta-endorphin correlated to VO2max (r = -0.76), peak rate-pressure product (r = -0.60) and exercise time (r = -0.56), then progressively increasing from class A to C. After exercise, beta-endorphin plasma levels increased respectively to 6.42 +/- 3.44 pmol/L (p < 0.001 vs baseline) in patients, and to 5.46 +/- 2.14 pmol/L (p < 0.001 vs baseline and NS vs patients) in normals. In patients, the release during exercise of beta-endorphin (exercise - baseline/baseline x 100) correlated to VO2max (r = 0.82), peak rate-pressure product (r = 0.64) and exercise time (r = 0.55), then progressively decreasing from class A to C. At multivariate analysis beta-endorphin release showed the greater correlation to exercise capacity parameters. CONCLUSIONS: In heart failure patients, beta-endorphin plasma levels are elevated at rest and its release during exercise is reduced in relation to functional impairment.

Adult↗
PubMed1987

Conventional and high frequency controlled mechanical ventilation in patients with left ventricular dysfunction and pulmonary edema.

The cardiopulmonary effects of conventional controlled mechanical ventilation (CMV), high frequency controlled mechanical ventilation (HFV), and intermittent mandatory ventilation (IMV) were compared in nine patients with ischemic left ventricular dysfunction and pulmonary edema. Ventilatory support during IMV and CMV was adjusted by changing the ventilator rate while tidal volume was maintained at 12 ml/kg. HFV was produced at a frequency of 100 cycles/min and an I/E ratio of 1:2. End-expiratory airway pressure and inspired oxygen concentration were maintained constant. The three ventilatory modes produced similar mean airway, transpulmonary, and intra-thoracic pressures. Mechanical control of respiration required hyperventilation during both CMV and HFV. Arterial blood oxygenation, heart rate, vascular pressures, cardiac output, and myocardial ischemia were unaffected by the changes in ventilation. Decreased arteriovenous oxygen content difference (p less than 0.05) and increased mixed venous oxygen content (p less than 0.05) suggested improved systemic blood flow during IMV. Controlled ventilation by conventional means or with a high frequency technique had no detectable advantage over partial ventilatory support with IMV during cardiopulmonary failure stabilized with vasoactive therapy and continuous positive airway pressure.

Aged↗
PubMed1991

Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs.

Cardiac arrhythmias are generated as the result of disorders of automaticity or of impulse conduction. Regardless of the mechanism, calcium is likely to be involved, although calcium antagonists are rarely useful antiarrhythmics in ventricular arrhythmias. Myocardial cells that do not ordinarily initiate action potentials may do so when they are partially depolarized, giving rise to an ectopic focus. Early afterdepolarizations (EADs) are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations (DADs) are induced by Ca++ overloading. EADs may be the initiating mechanism of torsade de pointes, a complication of QT prolongation associated with quinidine therapy. Both in the animal model and in humans, treatment with magnesium, isoproterenol, or pacing, all of which suppress EADs, will also suppress torsade de pointes. Ventricular tachycardia is a manifestation of ordered re-entry, and may be exacerbated by antiarrhythmics, especially class 1c drugs. In the individual patient, prediction of proarrhythmia is not possible. The risk of proarrhythmia is increased in patients with episodes of sustained ventricular tachycardia or with significant left ventricular dysfunction.

Anti-Arrhythmia Agents↗
PubMed2000

Assessment of acute right ventricular dysfunction induced by right coronary artery occlusion using echocardiographic atrioventricular plane displacement.

Right ventricular (RV) systolic function analysis by echocardiography has traditionally required RV endocardial border definition with subsequent tracing and is often inaccurate or impossible in technically poor studies. The atrioventricular plane displacement (AVPD) method attempts to use the descent of the tricuspid annular ring, a reflection of the longitudinal shortening of the right ventricle, as a surrogate marker for RV systolic function. We hypothesized that RV ischemia induced during right coronary artery occlusion proximal to the major right ventricular branches would result in severe right ventricular systolic dysfunction detectable by the AVPD method. During this pilot study, seven patients undergoing elective proximal RCA angioplasty had echocardiographic measurement of RV AVPD performed at baseline (i.e., immediately prior to RCA balloon inflation), during the last 30 seconds of first RCA balloon inflation, and at 1 minute after balloon deflation (recovery). Lateral and medial RV AVPD were significantly reduced from baseline values during intracoronary balloon inflation. (Lateral: 2.45 cm +/- 0.22 vs 1.77 cm +/- 0.13, P < 0.001; medial: 1.46 cm +/- 0.37 vs 1.28 cm +/- 0.32, P < 0.05). Additionally, lateral and medial RV AVPD significantly returned towards baseline values during recovery. (Lateral: 2.39 cm +/- 0.20, P < 0.001; medial: 1.58 cm +/- 0.27, P = 0.01). At baseline, all lateral RV AVPD values were > 2.0 cm, whereas during balloon inflation all were < 2.0 cm. No such clear distinction was found in medial RV AVPD values. Proximal RCA angioplasty is associated with a significant reduction in lateral and medial RV AVPD. Thus RV AVPD may serve as a marker for RV systolic dysfunction.

Acute Disease↗
PubMed1992

Reversible and irreversible left ventricular dysfunction after acute myocardial infarction.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Tc-99m tetrofosmin tomography after nitrate administration in patients with ischemic left ventricular dysfunction: relation to metabolic imaging by PET.

BACKGROUND: In patients with ischemic left ventricular (LV) dysfunction, myocardial perfusion imaging after nitrate administration may improve the identification of dysfunctional but viable myocardium. This study was designed to assess the relationship between tetrofosmin uptake after nitrate administration and metabolic activity as assessed by positron emission tomography (PET) in patients with ischemic LV dysfunction. METHODS AND RESULTS: Thirty-six patients with chronic myocardial infarction and LV dysfunction (ejection fraction, 35% +/- 6%) underwent resting technetium 99m tetrofosmin single photon emission computed tomography (SPECT) imaging under control conditions (baseline) and after sublingual administration of 10 mg isosorbide dinitrate. Within 1 week, all patients underwent metabolic PET imaging with fluorine 18-fluorodeoxyglucose. Tetrofosmin uptake and metabolic activity were measured in 13 segments/patient. Regional LV function was assessed in corresponding segments by echocardiography. On baseline tetrofosmin imaging, 53 (40%) of the 131 akinetic or dyskinetic segments had reduced (<55% of peak activity) tracer uptake. Of these segments, 14 (26%) showed enhanced tetrofosmin uptake after nitrate administration (>/=10% vs baseline) and the remaining 38 (74%) did not change. The sensitivity and specificity of baseline tetrofosmin SPECT for detecting preserved metabolic activity were 69% and 86%, respectively. After nitrate administration, the sensitivity was higher (81%, P <.05 vs baseline) whereas the specificity was not different (86%, P = not significant). Concordance between tetrofosmin SPECT and PET in differentiating viable and necrotic myocardium was observed in 94 (72%) of the 131 akinetic or dyskinetic segments at baseline (kappa = 0.35) and in 108 segments (82%) after nitrate administration (kappa = 0.53). CONCLUSIONS: After nitrate administration, tetrofosmin uptake in dysfunctional segments correlated with metabolic activity as assessed by fluorodeoxyglucose PET imaging better than baseline. Thus tetrofosmin SPECT after nitrate administration may improve the identification of ischemic but still viable myocardium in patients with chronic ischemic LV dysfunction.

Adult↗
PubMed1991

Coronary sinus occlusion: effect on ischemic left ventricular dysfunction and reactive hyperemia.

Pressure-controlled intermittent coronary sinus occlusion (PICSO) has been shown to reduce experimental infarct size. To examine the role of PICSO in limiting the consequences of brief ischemia on left ventricular function, we studied the effect of PICSO in nine open-chest anesthetized dogs. PICSO was performed using a pump-inflated, balloon-tipped catheter in the coronary sinus until coronary sinus occlusion pressure reached a plateau (10 +/- 3 seconds). The balloon was then rapidly deflated (2 seconds) and the cycle was repeated. Regional left ventricular function in the ischemic zone was assessed by sonomicrometry. Coronary blood flow was measured with a flow probe around the left anterior descending artery (LAD) proximal to an occluding suture. Measurements were obtained at baseline, during a 3-minute LAD occlusion, and for 10 minutes of reperfusion. In an additional five dogs, this sequence was repeated during an infusion of adenosine at a dose that abolished reactive hyperemia following LAD occlusion. The addition of PICSO beginning 15 minutes prior to ischemia and continuing throughout LAD occlusion and reperfusion did not prevent, reduce, or shorten ischemic left ventricular dysfunction. PICSO uniformly blunted reactive hyperemia during reperfusion. However, PICSO also reduced coronary blood flow during maximal vasodilatation achieved by adenosine infusion prior to LAD occlusion. Therefore, it is likely that PICSO decreases reactive hyperemia due to mechanical factors arising from venous engorgement rather than by reducing the ischemic stimulus causing vasodilation.

Animals↗
PubMed1998

Right Ventricular Dysfunction Secondary to Myocardial Ischemia Provoked by Stress Testing.

We present the cases of two patients, aged 59 and 85 years, who were evaluated with stress echocardiography for chest pain. Both patients developed dramatic echocardiographic findings consisting of severe right ventricular enlargement and hypokinesis, as well as enlargement of the right atrium at relatively low-level exercise. One patient collapsed with severe sinus bradycardia, junctional rhythm, ST elevation in the inferior leads, marked hypotension, and neck vein congestion. The other patient developed staggering and symptoms of hypoperfusion. In both patients, correction of critical proximal right coronary artery stenosis by angioplasty resulted in complete resolution of the right ventricular dysfunction on repeat stress testing. We conclude that in some patients, stress-induced myocardial ischemia may involve primarily the right ventricle with little or no evidence of ischemic changes in the left ventricle. An assessment of right ventricular function should be included in stress echocardiographic studies.

Journal Article↗