Left Ventricular Diastolic Filling Pattern at Doppler Echocardiography and Apoptotic Rate in Fatal Acute Myocardial Infarction

Sinagra, Gianfranco; Bussani, Rossana; Abbate, Antonio; Piro, Maddalena; Biondi‐Zoccai, Giuseppe; Kontos, Michael C.; Sabbadini, Gastone; Barresi, Elena; Crea, Filippo; Biasucci, Luigi M.; Aleksova, Aneta; Pinamonti, Bruno; Silvestri, Furio; Vetrovec, George W.; Baldi, Alfonso

doi:10.1016/j.amjcard.2006.08.025

Cited by 10 publications

(10 citation statements)

References 11 publications

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“…[7,8] In a canine experiment, comparing the effect of phenylephrine and norepinephrine in dogs with acute RV failure, only noradrenaline reduced PVR and increased coronary blood flow and consequently improved RV function and systemic hemodynamics. [6] Another study too found that noradrenaline increased SAP to a greater extent, with less increase in PAP compared to phenylephrine in patients with chronic pulmonary hypertension. [9] Phenylephrine is a synthetic selective α1-adrenergic agonist sympathomimetic amine with a strong vasoconstrictive, but minimal inotropic and chronotropic effect.…”

Section: Phenylephrine In Cardiac Surgery: Will It Have a Place?mentioning

confidence: 98%

“…[3,4] In clinical and animal studies of acute pulmonary hypertension, pulmonary artery pressure (PAP), and pulmonary vascular resistance (PVR) decreased when systemic arterial pressure (SAP) was raised with noradrenaline because subsequent increase in coronary perfusion pressure improved RV function and increased cardiac output. [5,6] The effect of phenylephrine is however debatable. [7,8] In a canine experiment, comparing the effect of phenylephrine and norepinephrine in dogs with acute RV failure, only noradrenaline reduced PVR and increased coronary blood flow and consequently improved RV function and systemic hemodynamics.…”

Section: Phenylephrine In Cardiac Surgery: Will It Have a Place?mentioning

confidence: 99%

“…Apoptosis is shown to reach a nadir at approximately 4 h postoperatively and persists for the first 2 days after cardiac surgery. [4][5][6] for the maintenance of blood pressure during spinal and inhalation anesthesia and for the treatment of vascular failure in shock, shock-like states, and drug-induced hypotension or hypersensitivity. However, α1 adrenergic receptors also exist in cardiomyocytes and their activation may lead to direct effects on the stressed myocardium.…”

Section: Introductionmentioning

confidence: 99%

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Phenylephrine postconditioning increases myocardial injury: Are alpha-1 sympathomimetic agonist cardioprotective?

Mourouzis¹,

Saranteas²,

Ligeret³

et al. 2014

Ann Card Anaesth

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Section: Phenylephrine In Cardiac Surgery: Will It Have a Place?mentioning

confidence: 98%

Section: Phenylephrine In Cardiac Surgery: Will It Have a Place?mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Phenylephrine postconditioning increases myocardial injury: Are alpha-1 sympathomimetic agonist cardioprotective?

Mourouzis¹,

Saranteas²,

Ligeret³

et al. 2014

Ann Card Anaesth

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“…Patients with biventricular enlargement had extremely high rates of cardiomyocyte apoptosis, compared to individuals who had no cardiac dilatation after MI [24]. Patients who died after an acute MI with severe postinfarction left ventricular (LV) diastolic dysfunction had significantly higher rates of apoptosis than those without LV dysfunction [33]. Thus, the amount of apoptosis is an important determinant of the amount of LV dysfunction which in turn is a major determinant of an unfavorable outcome pertaining to patient morbidity and mortality.…”

Section: Tunel-positive Cells May Include Apoptosis In Other Elementsmentioning

confidence: 99%

Apoptosis in Human Acute Myocardial Infarction: The Rationale for Clinical Trials of Apoptosis Inhibition in Acute Myocardial Infarction

Rabkin

2009

Scholarly Research Exchange

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The objective of the present review was to examine apoptosis in patients with acute myocardial infarction (MI) and to address (i) the prevalence of apoptosis in acute MI, (ii) techniques to determine apoptosis, (iii) time period from the onset of acute MI to the detection of apoptosis, (iv) criticisms about apoptosis in acute MI. A systematic literature search identified over 20 publications comprising over 400 patients. The prevalence of apoptosis varied from over 90% in nuclear imaging studies using annexin binding to 0.25% in an autopsy study using monoclonal antibody to single-stranded DNA. Apoptosis was present in 50-60% of infarcted hearts within 24 hours of MI (detected by Bax and activated caspase-3), 26% of myocytes in patients who died within 11 days of MI (pooled mean from 5 studies using only TUNEL staining), and 12% of the myocytes of patients who died, on average, 20 days after onset of MI (pooled mean from eight studies using dual staining with caspase-3 plus TUNEL). Criticisms of the TUNEL assay appear unjustified as TUNEL is at least 85% specific using caspase-3 activation as a marker of apoptosis. Taken together, DNA fragmentation on agarose gel electrophoresis, TUNEL staining of nuclei, caspase-3 activation, bcl-2 and Bax expression, and annexin V binding overwhelming support apoptotic cell death as an important component of MI. The amount of cardiac apoptosis correlates with the presence of heart failure and fatal arrhythmias. Heart failure as a complication of MI carries a high mortality and indicates the amount of myocardium lost during the infarct. Taken together, these findings suggest the need for clinical trials in acute MI to confirm whether inhibition of apoptosis can reduce patient morbidity and mortality.

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“…Stimulation of inflammatory mechanisms in acute coronary syndrome (ACS) is not limited to the microenviroment of the plaque and it involves circulating cell populations. In addition, apoptosis or programmed cell death play a critical role during immune responses of lymphocytes [2], while apoptosis of myocardial cells occurs after acute myocardial infarction (AMI) and it is correlated with impairment of left ventricular (LV) diastolic function [3]. In the present study we evaluated the lymphocyte activation and apoptosis during the acute and sub-acute phase of ST elevation myocardial infarction (STEMI).…”

mentioning

confidence: 99%

Lymphocyte activation and apoptotic process in acute coronary syndromes

Boutsikou¹,

Konstadoulakis²,

Tousoulis³

et al. 2011

International Journal of Cardiology

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Left Ventricular Diastolic Filling Pattern at Doppler Echocardiography and Apoptotic Rate in Fatal Acute Myocardial Infarction

Cited by 10 publications

References 11 publications

Phenylephrine postconditioning increases myocardial injury: Are alpha-1 sympathomimetic agonist cardioprotective?

Phenylephrine postconditioning increases myocardial injury: Are alpha-1 sympathomimetic agonist cardioprotective?

Apoptosis in Human Acute Myocardial Infarction: The Rationale for Clinical Trials of Apoptosis Inhibition in Acute Myocardial Infarction

Lymphocyte activation and apoptotic process in acute coronary syndromes

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