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      Alterations in Aortic Pressure and Coronary Blood Flow: Their Time Sequences with Induced Paroxysms of Ventricular Tachycardia in Normal and Impaired Myocardium

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          In an attempt to define more clearly the hemodynamic effects of paroxysmal tachycardia in their time sequence not only for the normal heart, we monitored coronary sinus flow (CSF), aortic mean pressure (AOMP), and coronary vascular resistance in 42 patients. They underwent stress testing of left ventricular function by paced ventricular tachycardia (VT 170/min); 13 patients had no heart disease (controls), 10 patients left ventricular hypertrophy, and 19 patients coronary artery disease (CAD). Up to the 6th s after the sudden start of VT, CSF was maintained during a 50% decrease in AOMP, while controls and hypertrophy patients with less pressure reduction (of 33 and 42%, respectively) showed a tendency to increase CSF. From the 12th to the 26th s of VT, a slight recovery of the low AOMP values took place, while CSF remained at or slightly below baseline levels. The steady state VT was characterized by further improved pressures and a CSF slightly above baseline even in CAD. Up to the 12th s after sudden stop of VT, aortic systolic pressure showed a steep increase (by 17, 13, and 8% for the three groups, respectively), while CSF dropped temporarily and after an upswing between the 12th and 26th s reached baseline levels together with AOMP. We conclude: (1) The rapidity of coronary response and its initial lag after changes of perfusion pressure are similar for normal and impaired myocardium; slight differences exist in quantity. (2) While with VT initiation perfusion pressure drops precipitously, CSF is maintained at baseline levels or slightly below even in CAD. (3) The quality of coronary hemodynamic adaptation to tachycardiac paroxysms in the impaired myocardium warrants the presence of additional operative mechanisms other than a reduced reduction in coronary vascular reserve capacity known in CAD and left ventricular hypertrophy.

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          Author and article information

          S. Karger AG
          07 November 2008
          : 69
          : 6
          : 313-325
          Kerckhoff-Klinik der Max-Planck-Gesellschaft Bad Nauheim, FRG
          173523 Cardiology 1982;69:313–325
          © 1982 S. Karger AG, Basel

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          Pages: 13
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