Mobilization of bone marrow-derived endothelial progenitor cells (EPC) might explain exercise-induced improvement of endothelial function. We assessed whether a maximal exercise bout could alter the number of circulating EPC in healthy subjects and whether this effect is related to their cardiovascular risk profile. Additionally, we investigated possible mediators of this effect, namely nitric oxide (NO) bioavailability and vascular endothelial growth factor (VEGF) release. Healthy subjects (group 1, n = 11; group 2, n = 14) performed a symptom-limited cardiopulmonary exercise test on a bicycle ergometer. Numbers of CD34+/kinase insert domain receptor (KDR)+ cells were determined by flow-cytometric analysis, either after magnetic separation of CD34+ cells (group 1) or starting from whole blood (group 2). Serum concentrations of VEGF and NO metabolites were measured by using ELISA. Following exercise, EPC increased by 76% (15.4 +/- 10.7 cells/ml vs. 27.2 +/- 13.7 cells/ml; P = 0.01) in group 1 and by 69% in group 2 (30.9 +/- 14.6 cells/ml vs. 52.5 +/- 42.6 cells/ml; P = 0.03). The increase in EPC correlated positively with LDL and total cholesterol/HDL ratio and negatively with peak oxygen consumption and oxygen consumption at anaerobic threshold. VEGF levels increased with exercise, with a strong trend toward significance (P = 0.055). NO levels remained unchanged. The present study demonstrates that a maximal bout of exercise induces a significant shift in CD34+ cells toward CD34+/KDR+ cells. This response was larger in subjects with a less favorable lipid profile.

Objective: To investigate the underlying mechanisms of a decreased coronary flow reserve after myocardial infarction (MI) by analysing the characteristics of the diastolic hyperaemic coronary pressure-flow relationship. Design: Prospective study. Setting: Tertiary care hospital. Patients: 68 patients with a recent MI and 27 patients with stable angina pectoris (AP; control group). Main outcome measures: The intercept with the pressure axis (the zero flow pressure or Pzf) and slope index of the pressure-flow relationship (SIPF) were calculated from the simultaneously recorded hyperaemic intracoronary blood flow velocity and aortic pressure after successful coronary stenting. Results: A stepwise increase in Pzf from AP (14.6 (8.0) mm Hg), over non-Q-wave MI (22.5 (9.1) mm Hg), to Q-wave MI (37.1 (12.9) mm Hg; p,0.001) was observed. Similar changes in Pzf were found in a reference artery perfusing the non-infarcted myocardium. Multivariate analysis showed that in both regions the left ventricular end-diastolic pressure (LVEDP) was the most important determinant of the Pzf. The SIPF was not statistically different in the treated vessel between patients with MI and AP, but was increased in MI patients with a markedly increased LVEDP. Conclusions: After an MI, the coronary pressure-flow relationship is shifted to the right both in the infarcted and in the non-infarcted remote myocardium, as shown by the increased Pzf. The correlation with Pzf suggests that elevated left ventricular filling pressures contribute to the impediment of myocardial perfusion in patients with infarction.A lthough the aim of current treatment strategies for myocardial infarction (MI) is to restore perfusion at the tissue level, important structural and functional changes in the microcirculation are present after restoration of epicardial vessel patency.1 These changes result in a decrease in the maximum achievable hyperaemic flow or a reduced coronary flow reserve (CFR) in the infarct area. [2][3][4] This impairment of the myocardial vasodilator capacity after MI has been reported to extend into the remote myocardium where a decreased CFR is observed as well. 2The hyperaemic diastolic coronary pressure-flow relationship and, in particular, its intercept with the pressure axis (the zero flow pressure or Pzf) have been extensively studied in animals.5 6 The advantage of this relationship over the CFR is that it provides a more comprehensive assessment of the properties of the microvascular compartment since it permits the assessment of coronary flow over a pressure range without the interference of cardiac contraction. Any decrease in the diastolic perfusion due to microvascular structural changes, microcirculatory functional alterations or effects of the surroundings (myocardial compartment) on the microvascular compartment results in a rightward displacement of the diastolic pressure-flow relationship in a pressure-flow diagram, and is reflected in an increase in the intercept pressure or Pzf.In humans, the coronary pressure-flow relationship ...

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Cannabis is a frequently used recreational drug that potentially imposes serious health problems. We report three cases where recent and/or chronic use of marijuana led to severe cardiac dysfunction. All three patients collapsed at home and required cardiopulmonary resuscitation (CPR) with initial restoration of spontaneous circulation (ROSC). The mechanism of the cardiovascular collapse was different in each case. The first case presented with asystole and was found to have diffuse coronary vasospasm on coronary angiography in the hours after acute cannabis abuse. In the second case, an acute anterior infarction with occlusion of both the right coronary artery (RCA) and the left anterior descendens (LAD) was observed in a young patient without known cardiovascular risks but with chronic cannabis abuse. The third case presented at home with ventricular fibrillation presumably caused by an acute coronary syndrome due to left anterior descending (LAD) artery occlusion. The hetero-anamnesis of the family reported that all three patients had recently used cannabis. Toxicological screening also showed no other substance abuse than cannabis. Using these three cases, we would like to illustrate that the widespread use of cannabis is not as innocent as is believed. Cannabis use can lead to severe cardiovascular problems and sudden death, not only in people at increased cardiovascular risk, but also in young people without any medical history or risk factors.