scholarly journals Early detection of acute transmural myocardial ischemia by the phasic systolic-diastolic changes of local tissue electrical impedance

2016 ◽  
Vol 310 (3) ◽  
pp. H436-H443 ◽  
Author(s):  
Esther Jorge ◽  
Gerard Amorós-Figueras ◽  
Tomás García-Sánchez ◽  
Ramón Bragós ◽  
Javier Rosell-Ferrer ◽  
...  

Myocardial electrical impedance is influenced by the mechanical activity of the heart. Therefore, the ischemia-induced mechanical dysfunction may cause specific changes in the systolic-diastolic pattern of myocardial impedance, but this is not known. This study aimed to analyze the phasic changes of myocardial resistivity in normal and ischemic conditions. Myocardial resistivity was measured continuously during the cardiac cycle using 26 different simultaneous excitation frequencies (1 kHz–1 MHz) in 7 anesthetized open-chest pigs. Animals were submitted to 30 min regional ischemia by acute left anterior descending coronary artery occlusion. The electrocardiogram, left ventricular (LV) pressure, LV dP/d t, and aortic blood flow were recorded simultaneously. Baseline myocardial resistivity depicted a phasic pattern during the cardiac cycle with higher values at the preejection period (4.19 ± 1.09% increase above the mean, P < 0.001) and lower values during relaxation phase (5.01 ± 0.85% below the mean, P < 0.001). Acute coronary occlusion induced two effects on the phasic resistivity curve: 1) a prompt (5 min ischemia) holosystolic resistivity rise leading to a bell-shaped waveform and to a reduction of the area under the LV pressure-impedance curve (1,427 ± 335 vs. 757 ± 266 Ω·cm·mmHg, P < 0.01, 41 kHz) and 2) a subsequent (5–10 min ischemia) progressive mean resistivity rise (325 ± 23 vs. 438 ± 37 Ω·cm at 30 min, P < 0.01, 1 kHz). The structural and mechanical myocardial dysfunction induced by acute coronary occlusion can be recognized by specific changes in the systolic-diastolic myocardial resistivity curve. Therefore these changes may become a new indicator (surrogate) of evolving acute myocardial ischemia.

1992 ◽  
Vol 73 (6) ◽  
pp. 2263-2273 ◽  
Author(s):  
J. Peters ◽  
P. Ihle

To evaluate, in the absence of lung inflation, the cardiovascular effects of single and repetitive pleural pressure increments induced by thoracic vest inflations and timed to occur during specific portions of the cardiac cycle, seven chronically instrumented dogs were studied. Reflexes and left ventricular (LV) performance were varied by autonomic blockade, circumflex coronary occlusion (with and without beta-blockade), or cardiac arrest. Single late systolic, but not early systolic, vest inflations significantly increased LV stroke volume both before (+12.4%) and after myocardial depression by coronary occlusion+beta-blockade (+18.5%) when performed after a period of apnea to control preload and rate. During vest inflations, LV and aortic pressures increased to a greater degree than esophageal pressure (by 51 vs. 39 mmHg, P = 0.0001). Lung inflations (26 trials in 3 dogs) during early or late systole failed to increase stroke volume, despite peak esophageal pressures of 11–26 mmHg. With autonomic reflexes intact, repetitive vest inflations coupled to early systole, late systole, or diastole induced a large (40%) but unspecific systemic flow increase. In contrast, during autonomic blockade, flow increased slightly (7.5%, P < 0.05) with late systolic compared with diastolic inflations but not relative to baseline. During coronary occlusion (with or without beta-blockade), no cycle-specific differences were seen, whereas matched vest inflations during cardiac arrest generated 20–30% of normal systemic flow. Thus only single late systolic thoracic vest inflations associated with large increments in pleural pressure increased LV emptying, presumably by decreasing LV afterload and/or focal cardiac compression. However, during myocardial ischemia and depression, coupling of vest inflation to specific parts of the cardiac cycle revealed no hemodynamic improvement, suggesting that benefits of this circulatory assist method, if any, are minor and may be restricted to conditions of cardiac arrest.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Amar M Salam ◽  
Kadhim Sulaiman ◽  
Robert O Bonow ◽  
Jassim Al-Suwaidi ◽  
Khalid AlHabib ◽  
...  

OBJECTIVES: No previous studies have specifically examined the effects of ethnicity on factors precipitating hospital admissions for heart Failure (HF). The aim of the current study was to identify factors precipitating HF hospitalizations peculiar to Middle-Eastern Arab and South Asian ethnicities using a large multinational multicenter Middle-Eastern HF registry in which these two ethnicities are most prevalent. METHODS: From February 2012 to November 2013, consecutive patients hospitalized with HF were enrolled from 47 hospitals in 7 Middle East countries. Identifiable factors contributing to HF hospitalization were pre-specified and captured at admission. Patients were divided into 2 groups according to ethnicity, Arabs and South Asians (referred to as Asians) and the 2 groups were compared. RESULTS: During the study period 5005 patients with HF were enrolled of whom 4989 patients were from the 2 ethnicities under study; 4516 Arabs (90.5%) and 473(9.5%) Asians with the mean age of 60 years for Arabs and 55 years for Asians. The mean left ventricular ejection fraction was 37 % for Arabs compared to 33.8 % for Asians, P=0.001. Among the precipitating factors studied, nonadherence to medications and infections were significantly more prevalent in Arabs compared to Asians (19.9% vs. 13.5% and 15.3% vs.8.5%, both P=0.001) whereas myocardial ischemia and uncontrolled hypertension were significantly more prevalent in Asians (40.4% vs. 25.9% and 11.6% vs.7.8%, both P=0.001). In both groups, however, myocardial ischemia and nonadherence to medications were the commonest two factors precipitating hospital admissions for HF (table). CONCLUSIONS: Our study identifies for the first time important ethnic related differences in precipitating factors for HF hospitalizations among Arabs and Asians living in the Middle-East. The current study underscores the need to consider ethnicity in studies of HF hospitalizations and HF outcomes.


2015 ◽  
pp. 311-317
Author(s):  
Fernando D. Dip ◽  
Alejandro Damonte ◽  
Gaston Quiche ◽  
Marcelo Damonte ◽  
Fernando M. Safdie ◽  
...  

Author(s):  
Daniel I. Ambinder ◽  
Kaustubha D. Patil ◽  
Hikmet Kadioglu ◽  
Pace S. Wetstein ◽  
Richard S. Tunin ◽  
...  

Background Pulseless electrical activity (PEA) is a common initial rhythm in cardiac arrest. A substantial number of PEA arrests are caused by coronary ischemia in the setting of acute coronary occlusion, but the underlying mechanism is not well understood. We hypothesized that the initial rhythm in patients with acute coronary occlusion is more likely to be PEA than ventricular fibrillation in those with prearrest severe left ventricular dysfunction. Methods and Results We studied the initial cardiac arrest rhythm induced by acute left anterior descending coronary occlusion in swine without and with preexisting severe left ventricular dysfunction induced by prior infarcts in non–left anterior descending coronary territories. Balloon occlusion resulted in ventricular fibrillation in 18 of 34 naïve animals, occurring 23.5±9.0 minutes following occlusion, and PEA in 1 animal. However, all 18 animals with severe prearrest left ventricular dysfunction (ejection fraction 15±5%) developed PEA 1.7±1.1 minutes after occlusion. Conclusions Acute coronary ischemia in the setting of severe left ventricular dysfunction produces PEA because of acute pump failure, which occurs almost immediately after coronary occlusion. After the onset of coronary ischemia, PEA occurred significantly earlier than ventricular fibrillation (<2 minutes versus 20 minutes). These findings support the notion that patients with baseline left ventricular dysfunction and suspected coronary disease who develop PEA should be evaluated for acute coronary occlusion.


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