Doppler echocardiography (DE) is becoming a powerful noninvasive tool for assessing left ventricular diastolic dysfunction after myocardial infarction (MI). Transmitral inflow DE measurements of early and late filling velocities, early to late ratio and early deceleration time correlate well with left ventricular filling pressure. Three abnormal filling patterns (impaired relaxation, pseudonormalization and restrictive) develop after MI, depending on infarct size. Pulmonary venous inflow DE contributes important additional diagnostic data and, when combined with transmitral DE, avoids potential confusion due to the pseudonormal pattern that develops in the presence of high left atrial pressure and impaired relaxation. Several studies indicate that these DE patterns correlate with progressively increasing functional impairment, and the restrictive transmitral pattern predicts heart failure and death among MI survivors. Further studies are needed to evaluate the effects of therapy on the DE patterns of diastolic dysfunction after MI.

We assessed the effects of the angiotensin II (Ang II) type 1 receptor (AT1-receptor) blocker, candesartan, (CN, 1 mg/kg i.v. over 30 minutes pre-ischaemia) alone or after intracoronary administration of Ang II type 2 receptor (AT2-receptor) blocker (PD 123319), protein kinase C (PKC) inhibitor (chelerythrine), endothelial nitric oxide (NO) synthase inhibitor (N(G)-monomethyl-L-arginine or L-NMMA), and bradykinin (BK) -B2 receptor inhibitor (HOE140) on in vivo left ventricular (LV) function and remodelling (echocardiograms/Doppler) and haemodynamics in 30 dogs with reperfused anterior infarction (90 minutes ischaemia, 120 minutes reperfusion), and ex vivo infarct size, AT1-receptor/AT2-receptor proteins and PKC(epsilon) (immunoblots), and cyclic guanosine 3', 5' monophosphate (cGMP, immunoassay). Compared with controls, CN inhibited the Ang II pressor response, reduced LV preload, improved LV systolic and diastolic function, limited LV remodelling, decreased infarct size, and increased AT2-receptor and PKC(epsilon) proteins in the infarct zone (IZ), and these responses were abrogated by PD 123319, chelerythrine, L-NMMA and HOE140. In addition, the increase in LV cGMP with CN was attenuated by PD 123319, L-NMMA and HOE140. The overall results suggest that AT2-receptor activation and signalling via BK, PKC(epsilon) and cGMP contribute to cardioprotection associated with AT1-receptor blockade during ischaemia-reperfusion injury.

To determine whether angiotensin II (Ang II) type 2 (AT2)-receptor activation associated with cardioprotection induced by Ang II type 1 (AT1)-receptor blockade during ischaemia-reperfusion (IR) might be reflected in increased AT 2-receptor, IP3-(1,4,5- inositol trisphosphate type 2) receptor and PKC-ε (protein kinase C-ε) proteins and tissue cGMP (cyclic guanosine monophosphate), we measured in vivo left ventricular (LV) systolic and diastolic function and remodelling (echocardiogram/Doppler) and haemodynamics, and ex vivo infarct size, AT1-/AT 2receptor, IP3-receptor and PKC-ε proteins (immunoblots) and cGMP (enzyme immunoassay) in dogs with reperfused anterior acute myocardial infarction (MI) (90-minute ischaemia, 120-minute reperfusion). Compared with controls (C, n=6) in vivo, candesartan (1 mg/kg i.v. over 30-minute pre-ischaemia, n=6) effectively inhibited the Ang II pressor response (Δ%, -14±22% vs. -80±11, p<0.003) and decreased preload (122±35 vs. -2±16%, p<0.01), improved LV systolic ejection fraction (-29±4 vs. -11±5, p<0.03) and diastolic function (E/A ratio, -25±7 vs. 33±13, p<0.004), decreased the extent of LV asynergy (26±20 vs. -31±10% LV, p<0.05) and limited acute LV remodelling (expansion index 19±6 vs. -3±5, p<0.05; thinning ratio -22±2 vs. -4±2, p<0.0003). Ex vivo, candesartan decreased infarct size (55±2 vs. 27±2% risk, p<0.001) and increased infarct zone (IZ) AT2 -receptor protein by 8-fold (but not AT1-receptor protein), IP3-receptor protein by 12-fold, PKC-ε protein by 5-fold and cGMP by 40%. Cardioprotective effects of AT1-receptor blockade on acute IR injury, LV function, and remodelling may also involve AT 2-receptor activation and downstream signalling via IP3-receptor, PKC-ε and cGMP.

A 62-year-old woman presented in the emergency department with new onset of dyspnea and clinical signs of cardiac tamponade. She had a history of cigarette smoking and a family history of adenocarcinoma, pancreatic and breast carcinoma. An emergency two-dimensional echocardiogram confirmed the diagnosis of cardiac tamponade. Therapeutic pericardiocentesis resulted in prompt relief. Cytology confirmed malignant glandular cells, consistent with a metastatic adenocarcinoma. Computerized chest tomography confirmed pulmonary involvement.

Background: We hypothesized that the cardioprotective effect of angiotensin II (AngII) type 1 receptor (AT,R) blockade during in vivo ischemia-reperfusion (IR) might be associated with an increase in AngII type 2 receptor (AT 2 R) protein, as well as 1,4,5-inositol trisphosphate type 2 receptor (IP 3 R) and protein kinase C ε , (PKC ε ) proteins and cyclic guanosine 3',5' monophosphate (cGMP). Methods and Results: We studied the effects of the AT 1 R blocker, candesartan, on in vivo left ventricular (LV) systolic and diastolic function and remodeling (echocardiogram/Doppler) and hemodynamics during canine reperfused anterior infarction (90-minute ischemia, 120-minute reperfusion), and ex vivo infarct size and AT 1 R/AT 2 R, IP 3 R, and PKC ε proteins (immunoblots), and cGMP (enzyme immunoassay). Compared with controls, candesartan (1 mg/kg intravenously over 30-minute preischemia) inhibited the AngII pressor response, decreased preload and afterload, improved LV systolic and diastolic function, limited LV remodeling, decreased infarct size (55% vs 27% risk; P < .000003), markedly increased AT 2 R, IP 3 R, and PKC ε proteins in the infarct zone, but not the AT,R protein, and increased infarct more than noninfarct cGMP. Conclusions: The overall results suggest that cardioprotective effects of AT 1 R blockade on acute IR injury might involve AT 2 R activation and downstream signaling via IP 3 R, PKC ε , and cGMP.