The mechanical interactions between heart contraction and perfusion of the heart are difficult to study in humans because of the restrictions in inducing changes in hemodynamic and cardiac mechanics parameters during catheterization. We hypothesize that the Valsalva maneuver can induce such alterations in the cardiac-coronary mechanical interaction and that these variations can be studied with the Wave Intensity Analysis. In order to interpret eventual changes in the wave intensity, a deep understanding of the effect of the Valsalva maneuver on the coronary circulation is needed. A particular attention has to be payed on the effect of the control of the microvascular resistance that is known to compensate for eventual alterations in the surrounding hemodynamic conditions when vessel tone is intact. In the catheterization laboratory, coronary pressure and flow velocity signals were recorded simultaneously by a new guidewire developed by Volcano Corporation. Aortic pressure, left ventricular pressure and ECG were acquired by the catheterization laboratory setup and recorded together with coronary hemodynamic signals. Left ventricular performance parameters were derived per beat from the noninvasive recording of the finger pressure using the Nexfin monitor developed by BMEYE B.V. In order to match the output data of coronary hemodynamic and left ventricular performance parameters, a dedicated program has been written in Delphi. An analysis of the per-beat data was performed in order to study the relative dependence of the parameters during the Valsalva maneuver. Pilot results of the Wave Intensity Analysis were obtained with an existing custom-made program also written in Delphi. Our study shows that the Valsalva maneuver caused a profound stress in the whole cardiovascular system. The well-known changes of the aortic pressure were transmitted also to the left ventricle and the coronary microcirculation. The data show that this stress caused a small but significant decrease in the flow velocity. As expected, the microvascular resistance varied with the same pattern as the coronary pressure trying to keep the flow constant. With respect to the decrease in stroke volume, cardiac output and contractility, the left ventricular performance was strongly compromised: pulse pressure generation and cardiac contraction were almost annulled. The decrease in systolic left ventricular pressure of almost 40% and the 2 fold increase in the end-diastolic left ventricular pressure confirm the decrease in the pumping action. Consequentially, the oxygen consumption of the heart decreased to 40% of the baseline level but only after an initial increase at the onset of the strain by 10%. The results also show that the timing of variation of the parameters was not the same. Especially the left ventricular end-diastolic pressure changed more rapidly than the perfusion pressure. Pilot results on Wave Intensity Analysis (WIA) show that the Valsalva maneuver gave rise to changes in the Wave Intensity pattern suggesting that the speed of the reflected waves has indeed been altered. Our results agree with previous studies that reveal a slight decrease in the flow velocity due to the Valsalva maneuver. Nevertheless, our results contradict the belief that ascribes the decrease in flow velocity to the decrease in oxygen consumption. We assume that the flow decrease is due to mechanical factors, especially the rise of left ventricular end-diastolic pressure. The results shown on WIA are pilot results and some work is still needed in this direction to obtain more information on the coronary-cardiac interaction. However, these results give confidence about the use of the Valsalva maneuver as an intervention affecting external parameters and thus they are useful in the study of coronary-cardiac interaction in humans.