Physical conditioning has been suggested as a useful adjunct or alternative to pharmacologic therapy in the treatment of borderline or mild hypertension. This recommendation stems from numerous studies that have demonstrated modest decreases in blood pressure in hypertensive individuals. Exercise guidelines should be based on preliminary exercise testing and modified to accommodate those patients who are taking a variety of antihypertensive medications. Although pure isometric exercise is generally contraindicated in hypertensive patients, potentially valuable training activities that involve a substantial static component, including arm crank ergometry and mild-to-moderate load weight training, probably requires individual assessment.

To evaluate the cardiac demands of hunting deer, continuous ambulatory electrocardiograms were obtained in men with and without coronary artery disease (CAD) and compared with their responses to maximal treadmill testing. A volunteer sample of 25 middle-aged men (mean +/- SD 55 +/- 7 years of age), 17 of whom had known CAD, completed the study. Peak heart rate (HR) during 7 different deer hunting activities was expressed as the mean percentage of the maximal HR (HRmax) attained during treadmill testing. Periods of sustained sinus tachycardia were identified. Arrhythmias and ST-segment depression during deer hunting that were not apparent during treadmill testing were documented. Overall, 22 of 25 subjects demonstrated HR responses >85% HRmax for 1 to 65 minutes. Ten subjects exceeded the HRmax achieved during treadmill testing for 1 to 5 minutes. The relative HR response during ambulatory activity in the field was inversely related to cardiorespiratory fitness, expressed as METs (r = -0.59; p = 0.0020). Three subjects had ischemic electrocardiograms during deer hunting, but not during treadmill testing. Complex arrhythmias in the field not detected by treadmill testing included ventricular bi-trigeminy, ventricular couplets, and 8 runs of ventricular tachycardia (3 to 28 beats) in 3 subjects with documented CAD. In conclusion, deer hunting can evoke sustained HRs, ischemic ST-segment depression, and threatening ventricular arrhythmias in excess of those documented during maximal treadmill testing. The strenuous nature of deer hunting coupled with presumed hyperadrenergia and superimposed environmental stresses may contribute to the excessive cardiac demands associated with this activity.

Journal of Interventional CardiologyVolume 14, Issue 5 p. 491-492 Free to Read HEART Group Notification Regarding “Management of Potential Conflict of Interest” GERALD C. TIMMIS M.D., F.A.C.C, F.A.H.A., F.S.C.A.I., GERALD C. TIMMIS M.D., F.A.C.C, F.A.H.A., F.S.C.A.I. Editor-in-ChiefSearch for more papers by this author GERALD C. TIMMIS M.D., F.A.C.C, F.A.H.A., F.S.C.A.I., GERALD C. TIMMIS M.D., F.A.C.C, F.A.H.A., F.S.C.A.I. Editor-in-ChiefSearch for more papers by this author First published: 08 June 2007 https://doi.org/10.1111/j.1540-8183.2001.tb00363.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume14, Issue5October 2001Pages 491-492 RelatedInformation

ObjectiveTo elicit a criterion elevation (>10%) in resting heart rate (HR) with training overstress, and subsequently test the hypothesis that such “reversed bradycardia” (RB) negatively affects running performance. DesignProspective before-and-after intervention with a comparison group. SettingGeneral community. Participants21 healthy male marathon runners. InterventionVoluntary doubling of training miles on 14 consecutive days. Main Outcome MeasuresLeft ventricular (LV) function by echocardiography, HR, and plasma epinephrine (PE) at rest and during submaximal exercise, and 15 km road run performance. ResultsTwo days after the training overstress, 12 runners met the criterion (RB group), showing an average elevation in resting HR of 16% (range: 11 to 23%). The RB group also exhibited hyperkinetic LV shortening (p < 0.05), elevated exercise HR (p < 0.001), increased PE at rest and during exercise (p < 0.05), and reduced 15 km performance (p < 0.05). The other nine runners who maintained a stable resting HR during the intervention showed no significant outcome changes. ConclusionsIn addition to muscular overuse, heightened sympathetic drive likely contributed to the observed reversal of bradycardia. The development of this stress-related cardiac perturbation was associated with a decrement in running performance, confirming the hypothesis.

Procainamide is a class IA antiarrhythmic drug indicated for the treatment of life-threatening or symptomatic ventricular arrhythmias. The current sustained-release formulation requires 6-hour dosing (qid). To improve patient compliance, a new sustained-release formulation for twice-daily (bid) administration has been developed (Procanbid, Parke-Davis). This study assesses the pharmacologic equivalence of the bid and qid formulations in the suppression of symptomatic ventricular premature depolarizations (VPDs). Fourteen centers enrolled a total of 99 patients with frequent symptomatic VPDs (average ≥20 VPDs/hr) who previously responded to and tolerated the procainamide qid formulation. During the first week of the double-blind phase, patients were randomized to either placebo or procainamide dosages of 1000, 2000, or 4000 mg/d (bid or qid formulations). In the second week, the patients were crossed over to the alternate formulation. Seventy-seven patients qualified for the primary activity analysis. The bid and qid formulations showed comparable effectiveness in the suppression of mean VPDs with a linear dose-response relationship. The VPD suppression was not attenuated towards the end of the dosing interval for either formulation. Sixty-eight of these patients entered an optional 1-year extension to receive the bid formulation. Thirty-seven (54%) patients had adverse effects. Of those, 15 (22%) had side effects considered treatment related. Most of the adverse events occurred during the first 6 weeks of treatment. Only a few patients (8%) withdrew as a consequence of treatment with the bid formulation. The overall safety profile of the bid formulation was similar to other formulations, and the procainamide bid formulation has a low proarrhythmic rate (`3%). In conclusion, the effectiveness of the twice-daily formulation of procainamide in the suppression of VPDs is comparable to the currently available qid formulation.

It is now widely agreed that platelets are intimately involved in and contribute to the pathogenesis of acute coronary thrombosis. Aspirin, a relatively weak inhibitor of platelet activation, saves lives when administered early after acute myocardial infarction and should be routinely used as lifelong therapy in patients with coronary atherosclerosis. Ticlopidine has a mechanism of action distinct from and additive to that of aspirin; it inhibits activation of platelets mediated by the agonist, adenosine diphosphate (ADP). The reduction in subacute coronary thrombosis attained by the use of combination therapy with aspirin and ticlopidine (for 2–4 weeks) after intracoronary stenting is further evidence of the role of platelets in mediating acute arterial thrombosis. Potent platelet agonists (like thrombin) can override the effect of aspirin and ticlopidine; therefore these agents are of limited efficacy. In contrast, inhibitors of the platelet glycoprotein (GP) IIb/IIIa receptor are potentially more potent inhibitors of adhesive platelet interaction and may therefore be effective in blocking adhesive platelet interactions irrespective of the activating agonist. The GPIIb/IIIa receptor mediates the bridging of platelets (platelet aggregation) via fibrinogen, thus allowing platelet to bind other platelets at the injured vessel wall. Antagonists of this receptor are thus capable of blocking the “effector function” by acting at a step that is downstream to platelet activation. By abrogating the final common pathway of platelet aggregation, antagonists of GPIIb/IIIa also affect the most proximal step in thrombin generation (that most efficiently occurs on the membrane surface provided by platelets). Accordingly, these agents can profoundly inhibit arterial thrombosis. The clinical use of the antibody fragment directed against the GPIIb/IIIa receptor (c7E3 Fab) has truly revolutionized the practice of interventional cardiology and has the potential to effectively treat heparin‐resistant intracoronary thrombosis. Synthetic antagonists of fibrinogen binding to the GPIIb/IIIa receptor (the “fibans”) are currently under initial clinical testing.

Journal of Interventional CardiologyVolume 10, Issue 6 p. 394-394 Free to Read FROM THE EDITOR… GERALD C. TIMMIS M.D., Corresponding Author GERALD C. TIMMIS M.D. From the William Beaumont Hospital, Royal Oak, MichiganAddress for reprints: Gerald C, Timmis, M.D., William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, MI 480703. Fax:(248)551-4199.Search for more papers by this author GERALD C. TIMMIS M.D., Corresponding Author GERALD C. TIMMIS M.D. From the William Beaumont Hospital, Royal Oak, MichiganAddress for reprints: Gerald C, Timmis, M.D., William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, MI 480703. Fax:(248)551-4199.Search for more papers by this author First published: 08 June 2007 https://doi.org/10.1111/j.1540-8183.1997.tb00062.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume10, Issue6December 1997Pages 394-394 RelatedInformation

Measuring maximal handgrip strength at the time of hospital discharge provides a simple method for prescribing load holding and load carrying and patients who have had myocardial infarction.

Berg, Thomas; Franklin, Barry A. FACSM; Gordon, Seymour; Timmis, Gerald C. Author Information

Franklin, Barn FACSM; Hogan, Pat; Bonzheim, Kim; Bakalyar, Donovan; Terrien, Ed; Gordon, Seymour; Timmis, Gerald C. Author Information

Franklin, Barry FACSM; Crause, Ingrid; Bonzheim, Kim; Berg, Tom; Fisher, Pam; Bakalyar, Donovan; Gordon, Seymour; Timmis, Gerald C Author Information

Bonzheim, Kim; Franklin, Barry FACSM; Hollingsworth, Victoria; Gordon, Seymour; Timmis, Gerald C Author Information

The authors determined whether aerobic exercise training at the peak heart rate (HR) achieved on low-level treadmill testing at the time of hospital discharge can improve functional capacity and measured maximum oxygen uptake (VO2max) in Phase II cardiac rehabilitation. Included in the study were 32 male patients recovering from uncomplicated myocardial infarction (Ml), all of whom took stable doses of propranolol. Submaximal treadmill tests using a modified Bruce protocol (final stage 1.7 mph, 10% grade; 4 metabolic units [METS]) were administered 9 ± 2 days after acute MI. From 30 to 63 days after Ml, 17 patients were randomized to an exercise group trained at monitored HR averaging 95 ± 3 beats/min, which closely matched their mean low-level test peak HR, whereas 15 control subjects performed only light activity at pulse rates averaging 79 ± 5 beats/min (P < 0.01 between groups). Otherwise, the two groups were similar in age, physical characteristics, cardiac status, low-level treadmill responses, maximal treadmill duration, and VO2maxdetermined 30 days after infarction. Treadmill duration was significantly higher (P < 0.05) in both groups upon revaluation 63 days after Ml. Maximum oxygen uptake increased significantly, from 19.8 ± 1.0 to 23.6 ± 1.3 mL/kg/min (19%, P < 0.01) in the exercise group. Maximum oxygen uptake also improved in the control group, from 19.4 ± 1.2 to 21.0 ± 1.1 mL/kg/min (8%), but this increase was not statistically significant. Maximum HR did not change significantly in either group. In the exercise group, peak values for HR and O2on low-level testing, (i.e., 94 ± 2 beats/min and 13.1 ± 1.1 mL/kg/min, respectively) averaged 66% ± 2% of VO2maxand 70 ± 3% of the maximum HR measured 30 days after MI. It was concluded that training at the low-level test peak HR before discharge was effective for improving treadmill duration and VO2,max. Completion of a submaximal treadmill protocol requiring 4 METS without symptom or sign limitations at time of hospital discharge elicits a peak HR that is valid for Phase II aerobic conditioning in patients receiving betablockers after Ml.

Berg, Tom; Bestervelt, Ron; Gordon, Seymour; Timmis, Gerald C.; Franklin, Barry A. FACSM Author Information